[{"id":"1p19q-codeletion-readout","name":"1p/19q codeletion","tldr":"Loss of one copy each of chromosome arms 1p and 19q, together with an IDH mutation, defines oligodendroglioma in the WHO 2021 classification. It predicts a slower course and a good response to chemotherapy, and separates oligodendroglioma from astrocytoma.","route":"/biomarkers/1p19q-codeletion-readout/","kind":"biomarker","sub":"Genome-wide readout","facets":{"kind":["Biomarker"],"cancers":["Oligodendroglioma, IDH-mutant and 1p/19q-codeleted","Glioma & glioblastoma","Astrocytoma, IDH-mutant"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Oligodendroglioma, IDH-mutant and 1p/19q-codeleted","href":"/cancers/oligodendroglioma/","tip":"Oligodendroglioma is the adult brain tumour most responsive to chemotherapy. It is recognised by an IDH mutation together with loss of parts of chromosomes 1 and 19, and after surgery it is treated with radiotherapy plus the PCV drug combination, or, for small grade 2 tumours, with vorasidenib or watchful waiting."},{"label":"Glioma & glioblastoma","href":"/cancers/glioblastoma/","tip":"Gliomas are now diagnosed by molecular class, and three classes got their first targeted drugs in 2024-25 (vorasidenib for IDH-mutant glioma, tovorafenib for BRAF-altered paediatric glioma, dordaviprone for H3 K27M). Glioblastoma is the hardest to treat: surgery, radiotherapy with temozolomide and tumour treating fields are its backbone, with CAR-T into the brain and focused ultrasound in trials."},{"label":"Astrocytoma, IDH-mutant","href":"/cancers/idh-mutant-astrocytoma/","tip":"IDH-mutant astrocytoma is the slow-growing form of adult glioma, defined by a mutation in the IDH1 or IDH2 gene that makes the tumour produce a chemical which rewires its own cells. Surgery first, and then either watchful waiting, the new pill vorasidenib, or radiotherapy with chemotherapy, depending on grade and how much tumour is left."}],"tags":[{"label":"glioma","href":"/tagged/glioma/","tip":"Every record tagged glioma."},{"label":"no-approval","href":"/tagged/no-approval/","tip":"Every record tagged no-approval."}]},"sortKeys":{"year":0}},{"id":"pd-ligand-9p24-alteration","name":"9p24.1 alteration of the PD-1 ligand loci","tldr":"An extra stretch of chromosome 9 that carries both of the molecules a tumour uses to switch off T cells, plus the enzyme that turns them up further. Nearly every classical Hodgkin lymphoma has it, which is why checkpoint drugs work so well there and so poorly in most other lymphomas.","route":"/biomarkers/pd-ligand-9p24-alteration/","kind":"biomarker","sub":"Genome-wide readout","facets":{"kind":["Biomarker"],"cancers":["Hodgkin lymphoma","Primary mediastinal (thymic) large B-cell lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Hodgkin lymphoma","href":"/cancers/hodgkin-lymphoma/","tip":"Hodgkin lymphoma is one of the most curable cancers, where the goal is now to cure with less toxicity, using brentuximab and, from 2026, first-line nivolumab."},{"label":"Primary mediastinal (thymic) large B-cell lymphoma","href":"/cancers/primary-mediastinal-b-cell-lymphoma/","tip":"Primary mediastinal B-cell lymphoma is a fast-growing lymphoma of the thymus behind the breastbone that mostly affects young women. Immunochemotherapy cures about nine in ten, radiotherapy can now be skipped when the end-of-treatment scan is clear, and PD-1 antibodies and CAR-T cells rescue many of those who relapse."}],"tags":[{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"akt1-e17k","name":"AKT1 E17K mutation","tldr":"AKT1 E17K is a single hotspot mutation, in about 3 to 5 percent of hormone-receptor-positive breast cancers, that switches on the AKT kinase directly. It is one of the three alterations that qualify a patient for capivasertib.","route":"/biomarkers/akt1-e17k/","kind":"biomarker","target":{"id":"akt","name":"AKT","targetClass":"kinase","tldr":"AKT is a central survival kinase downstream of PI3K, blocked by capivasertib in breast and now prostate cancer."},"sub":"AKT1/2/3","facets":{"kind":["Biomarker"],"cancers":["HR-positive / HER2-negative breast cancer","Endometrial cancer","Triple-negative breast cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Endometrial cancer","href":"/cancers/endometrial/","tip":"The gynaecological cancer where immunotherapy has had the biggest impact, guided by molecular classification."},{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."}],"tags":[{"label":"pi3k","href":"/tagged/pi3k/","tip":"Every record tagged pi3k."}]},"sortKeys":{"year":0}},{"id":"alk-fusion","name":"ALK fusion (ALK-positive)","tldr":"An ALK fusion, usually EML4::ALK, is a swapped piece of chromosome 2 that turns the ALK kinase on permanently in about 4 percent of lung adenocarcinomas. Seven ALK inhibitors are approved for it, including alectinib after surgery.","route":"/biomarkers/alk-fusion/","kind":"biomarker","target":{"id":"alk","name":"ALK","targetClass":"kinase","tldr":"ALK is a gene fusion driver in about 4 to 5% of non-small-cell lung cancers that responds to a succession of ALK inhibitor pills. Lorlatinib kept about 60% of patients progression-free at five years, alectinib is approved after surgery, and neladalkib targets compound resistance mutations."},"sub":"ALK","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Pancreatic ductal adenocarcinoma","KRAS wild-type pancreatic ductal adenocarcinoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Pancreatic ductal adenocarcinoma","href":"/cancers/pancreatic/","tip":"Almost every pancreatic tumour carries a KRAS mutation, and for the first time drugs against it work: daraxonrasib nearly doubled survival in previously treated disease in 2026. Pancreatic cancer has been the hardest common cancer to treat once advanced; that is what is starting to change."},{"label":"KRAS wild-type pancreatic ductal adenocarcinoma","href":"/cancers/kras-wild-type-pdac/","tip":"KRAS wild-type pancreatic cancer is the one in ten pancreatic cancers without the KRAS mutation that drives the rest. Instead many carry a different switched-on gene, often a fusion involving NRG1, NTRK, ALK, ROS1, FGFR2 or RET, or a BRAF change, and several of these have approved pills or antibodies, so these tumours must be sequenced with a test that detects fusions."}],"tags":[{"label":"fusion","href":"/tagged/fusion/","tip":"Every record tagged fusion."}]},"sortKeys":{"year":0}},{"id":"alk-resistance-mutation","name":"ALK kinase-domain resistance mutation (G1202R and the rest)","tldr":"After a lung cancer stops responding to an ALK-blocking tablet, finding a change inside the ALK protein itself is good news: it means the cancer still depends on ALK, and a later-generation tablet is likely to work. Finding none means the opposite.","route":"/biomarkers/alk-resistance-mutation/","kind":"biomarker","target":{"id":"alk","name":"ALK","targetClass":"kinase","tldr":"ALK is a gene fusion driver in about 4 to 5% of non-small-cell lung cancers that responds to a succession of ALK inhibitor pills. Lorlatinib kept about 60% of patients progression-free at five years, alectinib is approved after surgery, and neladalkib targets compound resistance mutations."},"sub":"ALK","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."}]},"sortKeys":{"year":0}},{"id":"ar-amplification","name":"AR amplification (gene and upstream enhancer)","tldr":"Extra copies of the gene for the androgen receptor. It is almost never present before hormone treatment and is found in about half of prostate cancers that have become resistant to it, which is why the stage the sample was taken at matters more than the result itself.","route":"/biomarkers/ar-amplification/","kind":"biomarker","target":{"id":"androgen-receptor","name":"Androgen receptor","targetClass":"nuclear-receptor","tldr":"The hormone switch that drives prostate cancer, attacked by castration and by pills that block the receptor."},"sub":"AR","facets":{"kind":["Biomarker"],"cancers":["Prostate cancer","Metastatic castration-resistant prostate cancer","Metastatic hormone-sensitive prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."},{"label":"Metastatic hormone-sensitive prostate cancer","href":"/cancers/prostate-mhspc/","tip":"Metastatic hormone-sensitive prostate cancer is disease that has spread but still responds to lowering testosterone. Hormone therapy alone is no longer enough: adding an androgen receptor inhibitor, and docetaxel for high-volume disease, lengthens life by years."}],"tags":[{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."}]},"sortKeys":{"year":0}},{"id":"ar-ligand-binding-domain-mutation","name":"AR ligand-binding-domain mutation (L702H, W742C, H875Y, T878A, F877L)","tldr":"A change in the part of the androgen receptor that hormone drugs attach to. Depending on which change it is, another hormone the man is already taking can switch the receptor on, or the blocking drug can start behaving as an activating one.","route":"/biomarkers/ar-ligand-binding-domain-mutation/","kind":"biomarker","target":{"id":"androgen-receptor","name":"Androgen receptor","targetClass":"nuclear-receptor","tldr":"The hormone switch that drives prostate cancer, attacked by castration and by pills that block the receptor."},"sub":"AR","facets":{"kind":["Biomarker"],"cancers":["Prostate cancer","Metastatic castration-resistant prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."}],"tags":[{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."}]},"sortKeys":{"year":0}},{"id":"ar-v7-splice-variant","name":"AR-V7 splice variant","tldr":"AR-V7 is a shortened androgen receptor that lacks the part hormone drugs bind, so it stays active without testosterone. Found in circulating tumour cells, it predicts poor response to abiraterone and enzalutamide, but no label uses it yet.","route":"/biomarkers/ar-v7-splice-variant/","kind":"biomarker","target":{"id":"androgen-receptor","name":"Androgen receptor","targetClass":"nuclear-receptor","tldr":"The hormone switch that drives prostate cancer, attacked by castration and by pills that block the receptor."},"sub":"AR","facets":{"kind":["Biomarker"],"cancers":["Metastatic castration-resistant prostate cancer","Prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."},{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."}],"tags":[{"label":"prostate","href":"/tagged/prostate/","tip":"Every record tagged prostate."},{"label":"no-approval","href":"/tagged/no-approval/","tip":"Every record tagged no-approval."}]},"sortKeys":{"year":0}},{"id":"b7-h3-expression","name":"B7-H3 (CD276) expression","tldr":"B7-H3 is an immune checkpoint protein overexpressed on small-cell lung, prostate and many solid tumours. Ifinatamab deruxtecan is in phase 3 for small-cell lung cancer without an expression cut-off; nothing is approved.","route":"/biomarkers/b7-h3-expression/","kind":"biomarker","target":{"id":"b7h3","name":"B7-H3","targetClass":"surface-antigen","tldr":"B7-H3 is an immune checkpoint-like surface protein found on 60 to 70% of small-cell lung cancers and 80 to 90% of castration-resistant prostate cancers, with little on normal tissue. It is used as an ADC address, chiefly by ifinatamab deruxtecan, now in phase 3 in small-cell lung cancer; whether blocking its immune-dampening role adds anything beyond payload delivery is unresolved."},"sub":"CD276","facets":{"kind":["Biomarker"],"cancers":["Small-cell lung cancer","Extensive-stage small-cell lung cancer","Metastatic castration-resistant prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Small-cell lung cancer","href":"/cancers/sclc/","tip":"A fast-growing lung cancer. About a third of cases are confined to one side of the chest and are treated to cure with chemotherapy and radiotherapy together; the rest respond to chemotherapy and relapse quickly. After 30 years without progress, durvalumab consolidation, the T-cell engager tarlatamab and antibody-drug conjugates have each lengthened survival since 2024."},{"label":"Extensive-stage small-cell lung cancer","href":"/cancers/extensive-stage-sclc/","tip":"Small-cell lung cancer that has spread responds fast to chemotherapy but almost always returns within a year. Adding an immunotherapy antibody to first-line chemotherapy helps a minority live for years, and the T-cell engager tarlatamab, which points immune cells at the DLL3 protein on the cancer, has for the first time lengthened life after relapse."},{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"bcl2-g101v","name":"BCL2 G101V and the other venetoclax binding-site mutations","tldr":"A change in the pocket of the survival protein BCL-2 where venetoclax has to fit. The protein still works and the drug no longer binds it. It can be detected in blood months before the disease starts growing again.","route":"/biomarkers/bcl2-g101v/","kind":"biomarker","target":{"id":"bcl2","name":"BCL-2","targetClass":"other","tldr":"A protein that stops cells from self-destructing. Venetoclax removes that protection and has transformed leukaemia treatment."},"sub":"BCL2","facets":{"kind":["Biomarker"],"cancers":["Non-Hodgkin lymphoma","Mantle cell lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."},{"label":"Mantle cell lymphoma","href":"/cancers/mantle-cell-lymphoma/","tip":"An uncommon B-cell lymphoma driven by cyclin D1 that used to behave badly in almost everyone. BTK inhibitors, CAR-T and now BCL2 drugs have changed it from chemotherapy-plus-transplant to targeted combinations."}],"tags":[{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."},{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"bcl2-rearrangement","name":"BCL2 rearrangement, t(14;18)","tldr":"A swap of DNA that puts the survival gene BCL2 next to an antibody gene, so the cell makes far too much of a protein that stops it dying. It is the founding event of most follicular lymphomas and it happens in the bone marrow, often years before anything is wrong.","route":"/biomarkers/bcl2-rearrangement/","kind":"biomarker","target":{"id":"bcl2","name":"BCL-2","targetClass":"other","tldr":"A protein that stops cells from self-destructing. Venetoclax removes that protection and has transformed leukaemia treatment."},"sub":"BCL2","facets":{"kind":["Biomarker"],"cancers":["Follicular lymphoma","Diffuse large B-cell lymphoma","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Follicular lymphoma","href":"/cancers/follicular-lymphoma/","tip":"Follicular lymphoma is the most common slow-growing lymphoma, defined in about 85% of cases by a BCL2 translocation. Most people live with it for decades, treated only when it causes problems; it can be controlled repeatedly with anti-CD20 antibodies, chemotherapy, bispecifics or CAR-T but rarely cured, and a small share transform into an aggressive lymphoma each year."},{"label":"Diffuse large B-cell lymphoma","href":"/cancers/dlbcl/","tip":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive but curable lymphoma. CAR-T cures about 40% of relapsed patients, and off-the-shelf bispecifics are now approved."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."}],"tags":[{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"bcma-expression","name":"BCMA expression","tldr":"BCMA is the plasma-cell antigen behind the myeloma bispecifics and CAR-T cells. None of their labels requires a BCMA test; expression is near-universal, and loss through BCMA gene deletion is a documented escape route.","route":"/biomarkers/bcma-expression/","kind":"biomarker","target":{"id":"bcma","name":"BCMA","targetClass":"surface-antigen","tldr":"BCMA is a survival receptor on plasma cells, and the target that made CAR-T and bispecifics work in multiple myeloma."},"sub":"TNFRSF17","facets":{"kind":["Biomarker"],"cancers":["Multiple myeloma","Relapsed or refractory multiple myeloma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Multiple myeloma","href":"/cancers/multiple-myeloma/","tip":"Multiple myeloma is a plasma-cell cancer with more new drug classes than any other: proteasome inhibitors, IMiDs, CD38 antibodies, BCMA CAR-T, bispecifics, and an ADC."},{"label":"Relapsed or refractory multiple myeloma","href":"/cancers/myeloma-relapsed-refractory/","tip":"Myeloma almost always returns, and each return is harder to treat. Two kinds of immune therapy aimed at the BCMA protein on myeloma cells, CAR-T cells (KarMMa-3, CARTITUDE-4) and off-the-shelf bispecific antibodies (MajesTEC), now give deep remissions after other drugs fail, and a second target, GPRC5D, gives another option."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"bcr-abl1-t315i","name":"BCR::ABL1 T315I","tldr":"T315I is the gatekeeper mutation in the ABL1 kinase that defeats imatinib, dasatinib, nilotinib and bosutinib. Ponatinib and asciminib are the two drugs approved for it.","route":"/biomarkers/bcr-abl1-t315i/","kind":"biomarker","target":{"id":"bcr-abl","name":"BCR::ABL1 (Philadelphia chromosome)","targetClass":"kinase","tldr":"The fusion that defines chronic myeloid leukaemia and a quarter of adult acute lymphoblastic leukaemia; the first cancer driver ever switched off by a pill."},"sub":"BCR-ABL1","facets":{"kind":["Biomarker"],"cancers":["Chronic myeloid leukaemia","Chronic myeloid leukaemia, chronic phase","Chronic myeloid leukaemia, accelerated and blast phase","Acute lymphoblastic leukaemia"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Chronic myeloid leukaemia","href":"/cancers/cml/","tip":"Chronic myeloid leukaemia is a blood cancer driven by a single fused gene, BCR-ABL1, and the model for oncogene-targeted treatment: imatinib in 2001 and the tyrosine kinase inhibitors that followed turned it into a condition most people live with long-term. About half of patients with a sustained deep molecular response can now stop treatment altogether."},{"label":"Chronic myeloid leukaemia, chronic phase","href":"/cancers/cml-chronic-phase/","tip":"Chronic-phase chronic myeloid leukaemia is the disease that imatinib turned from fatal into manageable: a daily pill blocks the BCR::ABL1 protein that drives it. Blood tests track the leukaemia gene to a millionth, newer pills such as asciminib (ASC4FIRST) reach deeper responses faster, and patients with years of undetectable disease can try stopping."},{"label":"Chronic myeloid leukaemia, accelerated and blast phase","href":"/cancers/cml-advanced-phase/","tip":"Chronic myeloid leukaemia can accelerate and then transform into an acute leukaemia called blast crisis. Tyrosine kinase inhibitors are given at full strength, combined with acute leukaemia chemotherapy in blast phase, to bring the disease back to chronic phase quickly enough for a donor stem cell transplant, the only treatment that cures it."},{"label":"Acute lymphoblastic leukaemia","href":"/cancers/all-leukemia/","tip":"Acute lymphoblastic leukaemia is the childhood cancer success story, and was the first disease treated with CAR-T and with a T-cell engager."}],"tags":[{"label":"cml","href":"/tagged/cml/","tip":"Every record tagged cml."},{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."}]},"sortKeys":{"year":0}},{"id":"bcr-abl1-transcript","name":"BCR::ABL1 transcript (Philadelphia chromosome, quantitative PCR)","tldr":"The BCR::ABL1 fusion is the Philadelphia chromosome that defines chronic myeloid leukaemia and some acute lymphoblastic leukaemia. Its transcript level in blood, on the international scale, is how response to tyrosine kinase inhibitors is measured and when treatment can be stopped.","route":"/biomarkers/bcr-abl1-transcript/","kind":"biomarker","target":{"id":"bcr-abl","name":"BCR::ABL1 (Philadelphia chromosome)","targetClass":"kinase","tldr":"The fusion that defines chronic myeloid leukaemia and a quarter of adult acute lymphoblastic leukaemia; the first cancer driver ever switched off by a pill."},"sub":"BCR-ABL1","facets":{"kind":["Biomarker"],"cancers":["Chronic myeloid leukaemia","Chronic myeloid leukaemia, chronic phase","Chronic myeloid leukaemia, accelerated and blast phase","Acute lymphoblastic leukaemia","Philadelphia chromosome-positive acute lymphoblastic leukaemia in children"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Chronic myeloid leukaemia","href":"/cancers/cml/","tip":"Chronic myeloid leukaemia is a blood cancer driven by a single fused gene, BCR-ABL1, and the model for oncogene-targeted treatment: imatinib in 2001 and the tyrosine kinase inhibitors that followed turned it into a condition most people live with long-term. About half of patients with a sustained deep molecular response can now stop treatment altogether."},{"label":"Chronic myeloid leukaemia, chronic phase","href":"/cancers/cml-chronic-phase/","tip":"Chronic-phase chronic myeloid leukaemia is the disease that imatinib turned from fatal into manageable: a daily pill blocks the BCR::ABL1 protein that drives it. Blood tests track the leukaemia gene to a millionth, newer pills such as asciminib (ASC4FIRST) reach deeper responses faster, and patients with years of undetectable disease can try stopping."},{"label":"Chronic myeloid leukaemia, accelerated and blast phase","href":"/cancers/cml-advanced-phase/","tip":"Chronic myeloid leukaemia can accelerate and then transform into an acute leukaemia called blast crisis. Tyrosine kinase inhibitors are given at full strength, combined with acute leukaemia chemotherapy in blast phase, to bring the disease back to chronic phase quickly enough for a donor stem cell transplant, the only treatment that cures it."},{"label":"Acute lymphoblastic leukaemia","href":"/cancers/all-leukemia/","tip":"Acute lymphoblastic leukaemia is the childhood cancer success story, and was the first disease treated with CAR-T and with a T-cell engager."}],"tags":[{"label":"cml","href":"/tagged/cml/","tip":"Every record tagged cml."}]},"sortKeys":{"year":0}},{"id":"braf-class-ii-iii","name":"BRAF class II and class III mutations (non-V600)","tldr":"Class II and III BRAF mutations sit outside codon 600 and signal as pairs (class II) or by leaning on RAS (class III). Approved BRAF inhibitors do not work on them, and no drug is yet approved for them; pan-RAF inhibitors are in trials.","route":"/biomarkers/braf-class-ii-iii/","kind":"biomarker","target":{"id":"braf","name":"BRAF","targetClass":"kinase","tldr":"BRAF is a signalling kinase mutated in half of melanomas; blocking it with two drugs at once became a template for targeted therapy."},"sub":"BRAF","facets":{"kind":["Biomarker"],"cancers":["Melanoma","Non-small-cell lung cancer","Colorectal cancer","Thyroid cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Melanoma","href":"/cancers/melanoma/","tip":"The skin cancer that proved immunotherapy works: half of advanced patients now live 10 years. Also the first with an approved TIL therapy, an oncolytic virus, and a positive phase 3 personalised vaccine."},{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Thyroid cancer","href":"/cancers/thyroid/","tip":"Thyroid cancer is usually curable with surgery and radioactive iodine, the original theranostic. Rare aggressive forms respond to RET and BRAF inhibitors."}],"tags":[{"label":"braf","href":"/tagged/braf/","tip":"Every record tagged braf."},{"label":"no-approval","href":"/tagged/no-approval/","tip":"Every record tagged no-approval."}]},"sortKeys":{"year":0}},{"id":"braf-fusion","name":"BRAF fusion or rearrangement","tldr":"A BRAF fusion joins another gene to the BRAF kinase, most often KIAA1549 in paediatric low-grade glioma. Tovorafenib is approved for children whose relapsed low-grade glioma carries a BRAF fusion or V600 mutation.","route":"/biomarkers/braf-fusion/","kind":"biomarker","target":{"id":"braf","name":"BRAF","targetClass":"kinase","tldr":"BRAF is a signalling kinase mutated in half of melanomas; blocking it with two drugs at once became a template for targeted therapy."},"sub":"BRAF","facets":{"kind":["Biomarker"],"cancers":["Paediatric low-grade glioma","Melanoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Paediatric low-grade glioma","href":"/cancers/paediatric-low-grade-glioma/","tip":"Paediatric low-grade gliomas are slow-growing brain tumours driven almost always by a single overactive signal, the MAPK pathway, most often through a BRAF gene change. Because the switch is known, pills that block it (dabrafenib with trametinib, and tovorafenib) now shrink tumours far more often than chemotherapy, and children are increasingly spared radiation to the developing brain."},{"label":"Melanoma","href":"/cancers/melanoma/","tip":"The skin cancer that proved immunotherapy works: half of advanced patients now live 10 years. Also the first with an approved TIL therapy, an oncolytic virus, and a positive phase 3 personalised vaccine."}],"tags":[{"label":"braf","href":"/tagged/braf/","tip":"Every record tagged braf."}]},"sortKeys":{"year":0}},{"id":"braf-v600e","name":"BRAF V600E (and V600K)","tldr":"V600E is the BRAF change that drives half of melanomas and many thyroid, bowel, lung and brain tumours. BRAF plus MEK inhibitors are approved for it in melanoma, lung, thyroid and, tumour-agnostically, any solid tumour; in bowel cancer it is treated with encorafenib and cetuximab.","route":"/biomarkers/braf-v600e/","kind":"biomarker","target":{"id":"braf","name":"BRAF","targetClass":"kinase","tldr":"BRAF is a signalling kinase mutated in half of melanomas; blocking it with two drugs at once became a template for targeted therapy."},"sub":"BRAF","facets":{"kind":["Biomarker"],"cancers":["Melanoma","Advanced melanoma","Colorectal cancer","Non-small-cell lung cancer","Thyroid cancer","Anaplastic thyroid cancer","Paediatric low-grade glioma","Metastatic cancer","Gallbladder cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Melanoma","href":"/cancers/melanoma/","tip":"The skin cancer that proved immunotherapy works: half of advanced patients now live 10 years. Also the first with an approved TIL therapy, an oncolytic virus, and a positive phase 3 personalised vaccine."},{"label":"Advanced melanoma","href":"/cancers/advanced-melanoma/","tip":"Advanced melanoma has spread beyond what surgery can remove, and it is the cancer in which immunotherapy first proved it could cure some people: about half of those given nivolumab with ipilimumab are alive ten years later. If immunotherapy fails, options include a cell therapy grown from the patient's own immune cells, a virus injected into the tumour, and targeted pills for BRAF-mutant disease."},{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"braf","href":"/tagged/braf/","tip":"Every record tagged braf."}]},"sortKeys":{"year":0}},{"id":"brca","name":"BRCA1 / BRCA2 (HRD)","tldr":"DNA repair genes. Inheriting a broken copy raises breast and ovarian cancer risk, but tumours that lose them become uniquely vulnerable to PARP inhibitors and platinum.","route":"/targets/brca/","kind":"target","target":{"id":"brca","name":"BRCA1 / BRCA2 (HRD)","targetClass":"tumor-suppressor","tldr":"DNA repair genes. Inheriting a broken copy raises breast and ovarian cancer risk, but tumours that lose them become uniquely vulnerable to PARP inhibitors and platinum."},"sub":"BRCA1, BRCA2","facets":{"kind":["Target"],"cancers":["Triple-negative breast cancer","Ovarian cancer","Prostate cancer","Pancreatic ductal adenocarcinoma","HR-positive / HER2-negative breast cancer","Gallbladder cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Target","tip":"The molecules drugs and tracers aim at."},"cancers":[{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."},{"label":"Ovarian cancer","href":"/cancers/ovarian/","tip":"Usually found late. PARP inhibitors transformed maintenance therapy, and ADCs against folate receptor and CDH6 are arriving for platinum-resistant disease."},{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Pancreatic ductal adenocarcinoma","href":"/cancers/pancreatic/","tip":"Almost every pancreatic tumour carries a KRAS mutation, and for the first time drugs against it work: daraxonrasib nearly doubled survival in previously treated disease in 2026. Pancreatic cancer has been the hardest common cancer to treat once advanced; that is what is starting to change."}],"tags":[{"label":"germline","href":"/tagged/germline/","tip":"Every record tagged germline."}]},"sortKeys":{"year":0}},{"id":"btk-c481s","name":"BTK resistance mutations: C481S, and L528W and T474I after the non-covalent inhibitors","tldr":"A change in the enzyme BTK at the exact point where the drug grips it. The enzyme keeps working and the drug no longer holds, which is the usual reason a BTK inhibitor stops working after it has been working well.","route":"/biomarkers/btk-c481s/","kind":"biomarker","target":{"id":"btk","name":"BTK (Bruton tyrosine kinase)","targetClass":"kinase","tldr":"The signalling enzyme that B-cell cancers use to survive. Blocking it turned chronic lymphocytic leukaemia into a disease controlled by a daily pill."},"sub":"BTK","facets":{"kind":["Biomarker"],"cancers":["Mantle cell lymphoma","Waldenström macroglobulinaemia","Non-Hodgkin lymphoma","Marginal zone lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Mantle cell lymphoma","href":"/cancers/mantle-cell-lymphoma/","tip":"An uncommon B-cell lymphoma driven by cyclin D1 that used to behave badly in almost everyone. BTK inhibitors, CAR-T and now BCL2 drugs have changed it from chemotherapy-plus-transplant to targeted combinations."},{"label":"Waldenström macroglobulinaemia","href":"/cancers/waldenstrom/","tip":"A slow lymphoma that makes an abnormal IgM antibody, causing thick blood, anaemia and nerve damage. Nearly all cases share one mutation (MYD88 L265P), and BTK inhibitors control it for years."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."},{"label":"Marginal zone lymphoma","href":"/cancers/marginal-zone-lymphoma/","tip":"Marginal zone lymphoma is a slow B-cell lymphoma that often grows where the body has been fighting a chronic infection: the stomach with Helicobacter pylori, the eye, the skin or the spleen. Curing the infection cures many early cases; the rest are treated with rituximab, chemotherapy or BTK inhibitors."}],"tags":[{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."},{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"met-overexpression","name":"c-Met protein overexpression (IHC 3+ in >= 50% of tumour cells)","tldr":"c-Met overexpression is a stain, not a gene change: strong (3+) membrane staining in at least half of tumour cells. It selects telisotuzumab vedotin, an antibody-drug conjugate, in previously treated non-squamous lung cancer.","route":"/biomarkers/met-overexpression/","kind":"biomarker","target":{"id":"met","name":"MET","targetClass":"kinase","tldr":"A receptor that is either mutated in some lung cancers or amplified as an escape route when other lung cancer drugs fail."},"sub":"MET","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"met","href":"/tagged/met/","tip":"Every record tagged met."}]},"sortKeys":{"year":0}},{"id":"cd19-expression","name":"CD19 expression (CD19-positive)","tldr":"CD19 is the B-cell surface protein that blinatumomab, CAR-T cells and several antibodies aim at. Blinatumomab's label requires CD19-positive leukaemia; the CAR-T labels assume it, and losing CD19 is the commonest way the disease escapes.","route":"/biomarkers/cd19-expression/","kind":"biomarker","target":{"id":"cd19","name":"CD19","targetClass":"surface-antigen","tldr":"CD19 is a marker on B cells and B-cell cancers, and was the target of the first CAR-T therapies ever approved."},"sub":"CD19","facets":{"kind":["Biomarker"],"cancers":["Acute lymphoblastic leukaemia","Relapsed and refractory acute lymphoblastic leukaemia in children","Diffuse large B-cell lymphoma","Follicular lymphoma","Mantle cell lymphoma","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Acute lymphoblastic leukaemia","href":"/cancers/all-leukemia/","tip":"Acute lymphoblastic leukaemia is the childhood cancer success story, and was the first disease treated with CAR-T and with a T-cell engager."},{"label":"Relapsed and refractory acute lymphoblastic leukaemia in children","href":"/cancers/all-paediatric-relapsed/","tip":"When childhood leukaemia comes back, chemotherapy alone cures fewer than half. Three immune treatments changed this: blinatumomab, which links the child's T-cells to leukaemia cells and beat chemotherapy in two trials; tisagenlecleucel, the first approved CAR T-cell therapy, which put over eight in ten pretreated children into remission; and the antibody-drug conjugate inotuzumab ozogamicin."},{"label":"Diffuse large B-cell lymphoma","href":"/cancers/dlbcl/","tip":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive but curable lymphoma. CAR-T cures about 40% of relapsed patients, and off-the-shelf bispecifics are now approved."},{"label":"Follicular lymphoma","href":"/cancers/follicular-lymphoma/","tip":"Follicular lymphoma is the most common slow-growing lymphoma, defined in about 85% of cases by a BCL2 translocation. Most people live with it for decades, treated only when it causes problems; it can be controlled repeatedly with anti-CD20 antibodies, chemotherapy, bispecifics or CAR-T but rarely cured, and a small share transform into an aggressive lymphoma each year."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."}]},"sortKeys":{"year":0}},{"id":"cd20-expression","name":"CD20 expression (CD20-positive)","tldr":"CD20 is the B-cell antigen rituximab made famous. Rituximab and obinutuzumab labels are written for CD20-positive lymphoma and leukaemia; the newer CD20 x CD3 bispecifics assume it.","route":"/biomarkers/cd20-expression/","kind":"biomarker","target":{"id":"cd20","name":"CD20","targetClass":"surface-antigen","tldr":"CD20 is a B-cell marker; rituximab against it was the first antibody approved for cancer, in 1997."},"sub":"MS4A1","facets":{"kind":["Biomarker"],"cancers":["Non-Hodgkin lymphoma","Diffuse large B-cell lymphoma","Follicular lymphoma","Chronic lymphocytic leukaemia","Mantle cell lymphoma","Marginal zone lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."},{"label":"Diffuse large B-cell lymphoma","href":"/cancers/dlbcl/","tip":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive but curable lymphoma. CAR-T cures about 40% of relapsed patients, and off-the-shelf bispecifics are now approved."},{"label":"Follicular lymphoma","href":"/cancers/follicular-lymphoma/","tip":"Follicular lymphoma is the most common slow-growing lymphoma, defined in about 85% of cases by a BCL2 translocation. Most people live with it for decades, treated only when it causes problems; it can be controlled repeatedly with anti-CD20 antibodies, chemotherapy, bispecifics or CAR-T but rarely cured, and a small share transform into an aggressive lymphoma each year."},{"label":"Chronic lymphocytic leukaemia","href":"/cancers/cll/","tip":"A slow leukaemia that no longer needs chemotherapy: BTK inhibitors and venetoclax control it for years, often in fixed-duration courses."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."}]},"sortKeys":{"year":0}},{"id":"cd22-expression","name":"CD22 expression (CD22-positive)","tldr":"CD22 is a second B-cell antigen, kept even when CD19 is lost. Inotuzumab ozogamicin is labelled for CD22-positive acute lymphoblastic leukaemia.","route":"/biomarkers/cd22-expression/","kind":"biomarker","target":{"id":"cd22","name":"CD22","targetClass":"surface-antigen","tldr":"CD22 is a B-cell surface protein and the docking site for the leukaemia ADC inotuzumab ozogamicin."},"sub":"CD22","facets":{"kind":["Biomarker"],"cancers":["Acute lymphoblastic leukaemia","Relapsed and refractory acute lymphoblastic leukaemia in children","Non-Hodgkin lymphoma","Diffuse large B-cell lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Acute lymphoblastic leukaemia","href":"/cancers/all-leukemia/","tip":"Acute lymphoblastic leukaemia is the childhood cancer success story, and was the first disease treated with CAR-T and with a T-cell engager."},{"label":"Relapsed and refractory acute lymphoblastic leukaemia in children","href":"/cancers/all-paediatric-relapsed/","tip":"When childhood leukaemia comes back, chemotherapy alone cures fewer than half. Three immune treatments changed this: blinatumomab, which links the child's T-cells to leukaemia cells and beat chemotherapy in two trials; tisagenlecleucel, the first approved CAR T-cell therapy, which put over eight in ten pretreated children into remission; and the antibody-drug conjugate inotuzumab ozogamicin."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."},{"label":"Diffuse large B-cell lymphoma","href":"/cancers/dlbcl/","tip":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive but curable lymphoma. CAR-T cures about 40% of relapsed patients, and off-the-shelf bispecifics are now approved."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."}]},"sortKeys":{"year":0}},{"id":"cd30-expression","name":"CD30 expression (CD30-positive)","tldr":"CD30 is the antigen of Hodgkin Reed-Sternberg cells and anaplastic large cell lymphoma. Brentuximab vedotin is labelled for Hodgkin lymphoma without a CD30 test and for peripheral T-cell lymphomas that express it.","route":"/biomarkers/cd30-expression/","kind":"biomarker","target":{"id":"cd30","name":"CD30","targetClass":"surface-antigen","tldr":"CD30 is a protein on the malignant Reed-Sternberg cells of Hodgkin lymphoma and on some T-cell lymphomas, and the address for the ADC brentuximab vedotin."},"sub":"TNFRSF8","facets":{"kind":["Biomarker"],"cancers":["Hodgkin lymphoma","Peripheral T-cell lymphomas","Cutaneous T-cell lymphoma","Primary mediastinal (thymic) large B-cell lymphoma","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Hodgkin lymphoma","href":"/cancers/hodgkin-lymphoma/","tip":"Hodgkin lymphoma is one of the most curable cancers, where the goal is now to cure with less toxicity, using brentuximab and, from 2026, first-line nivolumab."},{"label":"Peripheral T-cell lymphomas","href":"/cancers/peripheral-t-cell-lymphoma/","tip":"Peripheral T-cell lymphomas are lymphomas of T cells rather than B cells. They are rarer, more varied and, apart from a few subtypes, harder to treat than B-cell lymphomas; several new drugs help only defined subtypes."},{"label":"Cutaneous T-cell lymphoma","href":"/cancers/cutaneous-t-cell-lymphoma/","tip":"Cutaneous T-cell lymphoma is a family of nine lymphomas that start in the skin and mostly stay there, of which mycosis fungoides is by far the commonest. Most of them are long-term skin conditions managed over decades rather than cancers that are cured or not cured, and two of the nine are genuinely aggressive."},{"label":"Primary mediastinal (thymic) large B-cell lymphoma","href":"/cancers/primary-mediastinal-b-cell-lymphoma/","tip":"Primary mediastinal B-cell lymphoma is a fast-growing lymphoma of the thymus behind the breastbone that mostly affects young women. Immunochemotherapy cures about nine in ten, radiotherapy can now be skipped when the end-of-treatment scan is clear, and PD-1 antibodies and CAR-T cells rescue many of those who relapse."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."}]},"sortKeys":{"year":0}},{"id":"cd33-expression","name":"CD33 expression (CD33-positive)","tldr":"CD33 is a myeloid antigen on the blasts of about 90 percent of acute myeloid leukaemias. Gemtuzumab ozogamicin's label requires CD33-positive disease.","route":"/biomarkers/cd33-expression/","kind":"biomarker","target":{"id":"cd33","name":"CD33","targetClass":"surface-antigen","tldr":"CD33 is a myeloid surface marker on the blasts of 85 to 90% of acute myeloid leukaemias and on normal myeloid cells, so drugs against it also hit healthy marrow. It is the target of gemtuzumab ozogamicin, the first ADC ever approved (2000), withdrawn in 2010 and re-approved in 2017 at a lower fractionated dose."},"sub":"CD33","facets":{"kind":["Biomarker"],"cancers":["Acute myeloid leukaemia","Acute myeloid leukaemia in children"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"Acute myeloid leukaemia in children","href":"/cancers/aml-paediatric/","tip":"Acute myeloid leukaemia in children carries gene fusions rather than the mutations of ageing, is treated with four or five intensive courses of chemotherapy, and cures around two thirds of children. Adding gemtuzumab ozogamicin lowered relapse in the AAML0531 trial, and the menin inhibitor revumenib is the first targeted drug approved for the KMT2A-rearranged form common in young children."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."}]},"sortKeys":{"year":0}},{"id":"cd38-expression","name":"CD38 expression","tldr":"CD38 is on almost every myeloma cell, so daratumumab and isatuximab are given without testing for it. The stain matters afterwards: CD38 falls after treatment and can confuse flow cytometry and blood typing.","route":"/biomarkers/cd38-expression/","kind":"biomarker","target":{"id":"cd38","name":"CD38","targetClass":"surface-antigen","tldr":"CD38 is a myeloma surface enzyme and the target of daratumumab, which is now given as a quick under-the-skin injection."},"sub":"CD38","facets":{"kind":["Biomarker"],"cancers":["Multiple myeloma","Newly diagnosed multiple myeloma, transplant-eligible","Newly diagnosed multiple myeloma, transplant-ineligible","Relapsed or refractory multiple myeloma","Non-Hodgkin lymphoma","Peripheral T-cell lymphomas"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Multiple myeloma","href":"/cancers/multiple-myeloma/","tip":"Multiple myeloma is a plasma-cell cancer with more new drug classes than any other: proteasome inhibitors, IMiDs, CD38 antibodies, BCMA CAR-T, bispecifics, and an ADC."},{"label":"Newly diagnosed multiple myeloma, transplant-eligible","href":"/cancers/myeloma-transplant-eligible/","tip":"Fit patients with newly diagnosed myeloma receive four drugs at once, then their own stem cells are collected, they are given high-dose chemotherapy, the cells are returned and they continue on maintenance. Adding the CD38 antibody daratumumab to the three-drug backbone, tested in PERSEUS and CASSIOPEIA, means most patients now reach a state where no myeloma can be detected."},{"label":"Newly diagnosed multiple myeloma, transplant-ineligible","href":"/cancers/myeloma-transplant-ineligible/","tip":"Most people with newly diagnosed myeloma are too old or frail for a stem cell transplant. Combining a CD38 antibody with lenalidomide and dexamethasone (MAIA) and, for the fitter, with bortezomib as well (IMROZ), now keeps the disease away for around five years in many and lengthens life."},{"label":"Relapsed or refractory multiple myeloma","href":"/cancers/myeloma-relapsed-refractory/","tip":"Myeloma almost always returns, and each return is harder to treat. Two kinds of immune therapy aimed at the BCMA protein on myeloma cells, CAR-T cells (KarMMa-3, CARTITUDE-4) and off-the-shelf bispecific antibodies (MajesTEC), now give deep remissions after other drugs fail, and a second target, GPRC5D, gives another option."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"cd79b-itam-mutation","name":"CD79B ITAM mutation","tldr":"A change in the signalling tail of part of the B-cell receptor that leaves the receptor switched on without needing anything to bind it. It marks a group of large B-cell lymphomas that depend on that signal, and therefore on the enzyme BTK.","route":"/biomarkers/cd79b-itam-mutation/","kind":"biomarker","target":{"id":"cd79b","name":"CD79b","targetClass":"surface-antigen","tldr":"Part of the B-cell receptor found on nearly all B-cell lymphomas; the target of the ADC polatuzumab vedotin and a frequently mutated gene in brain and testicular lymphoma."},"sub":"CD79B","facets":{"kind":["Biomarker"],"cancers":["Diffuse large B-cell lymphoma","Primary CNS lymphoma","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Diffuse large B-cell lymphoma","href":"/cancers/dlbcl/","tip":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive but curable lymphoma. CAR-T cures about 40% of relapsed patients, and off-the-shelf bispecifics are now approved."},{"label":"Primary CNS lymphoma","href":"/cancers/primary-cns-lymphoma/","tip":"Primary CNS lymphoma is a lymphoma confined to the brain, eyes and spinal fluid. Unlike most brain tumours it is chemo-sensitive: high-dose methotrexate-based treatment cures a substantial minority, and consolidation with a stem-cell transplant has replaced whole-brain radiation for the fit."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."}],"tags":[{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"ceacam5","name":"CEACAM5","tldr":"The classic 'CEA' tumour marker measured in blood, also present on the cell surface where ADCs can reach it.","route":"/targets/ceacam5/","kind":"target","target":{"id":"ceacam5","name":"CEACAM5","targetClass":"surface-antigen","tldr":"The classic 'CEA' tumour marker measured in blood, also present on the cell surface where ADCs can reach it."},"sub":"CEACAM5","facets":{"kind":["Target"],"cancers":["Colorectal cancer","Non-small-cell lung cancer","Gastric & gastro-oesophageal junction cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Target","tip":"The molecules drugs and tracers aim at."},"cancers":[{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Gastric & gastro-oesophageal junction cancer","href":"/cancers/gastric/","tip":"A cancer with three new targets in five years: Claudin 18.2, FGFR2b, and HER2 with new ADCs, plus immunotherapy in first line."}],"tags":[{"label":"adc-target","href":"/tagged/adc-target/","tip":"Every record tagged adc-target."}]},"sortKeys":{"year":0}},{"id":"ceacam5-expression","name":"CEACAM5 expression","tldr":"CEACAM5 is the cell-surface form of the tumour marker CEA, high on many lung and bowel cancers. Tusamitamab ravtansine was tested in CEACAM5-high lung cancer but failed its phase 3 and no approval exists.","route":"/biomarkers/ceacam5-expression/","kind":"biomarker","target":{"id":"ceacam5","name":"CEACAM5","targetClass":"surface-antigen","tldr":"The classic 'CEA' tumour marker measured in blood, also present on the cell surface where ADCs can reach it."},"sub":"CEACAM5","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Colorectal cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"ctdna-tumour-fraction","name":"Circulating tumour DNA fraction (and what a negative plasma result means)","tldr":"How much of the DNA floating in a blood sample came from the cancer. Above a few per cent, a plasma test finds what a biopsy would find; below it, a negative result means the test could not see, not that there is nothing there.","route":"/biomarkers/ctdna-tumour-fraction/","kind":"biomarker","sub":"Genome-wide readout","facets":{"kind":["Biomarker"],"cancers":["Prostate cancer","Metastatic castration-resistant prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."}],"tags":[{"label":"prostate","href":"/tagged/prostate/","tip":"Every record tagged prostate."}]},"sortKeys":{"year":0}},{"id":"cldn18-2-expression","name":"Claudin 18.2 expression (>= 75% of tumour cells, moderate to strong)","tldr":"Claudin 18.2 is a tight-junction protein exposed on stomach cancer cells. Zolbetuximab requires at least 75 percent of tumour cells to stain moderately or strongly, the strictest expression threshold in any current label.","route":"/biomarkers/cldn18-2-expression/","kind":"biomarker","target":{"id":"cldn18-2","name":"Claudin 18.2","targetClass":"surface-antigen","tldr":"A tight-junction protein normally hidden in the stomach lining that becomes exposed in gastric and pancreatic cancers."},"sub":"CLDN18","facets":{"kind":["Biomarker"],"cancers":["Gastric & gastro-oesophageal junction cancer","Claudin 18.2-positive gastric cancer","Pancreatic ductal adenocarcinoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Gastric & gastro-oesophageal junction cancer","href":"/cancers/gastric/","tip":"A cancer with three new targets in five years: Claudin 18.2, FGFR2b, and HER2 with new ADCs, plus immunotherapy in first line."},{"label":"Claudin 18.2-positive gastric cancer","href":"/cancers/gastric-cldn18-2-positive/","tip":"Claudin 18.2 is a tight-junction protein normally hidden inside stomach lining cells that becomes exposed on the surface of many stomach cancers. Zolbetuximab, an antibody against it, added to chemotherapy lengthens survival in tumours that express it strongly, and antibody-drug conjugates and CAR-T cells against the same target are in trials."},{"label":"Pancreatic ductal adenocarcinoma","href":"/cancers/pancreatic/","tip":"Almost every pancreatic tumour carries a KRAS mutation, and for the first time drugs against it work: daraxonrasib nearly doubled survival in previously treated disease in 2026. Pancreatic cancer has been the hardest common cancer to treat once advanced; that is what is starting to change."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."}]},"sortKeys":{"year":0}},{"id":"ctdna-mrd-positive","name":"ctDNA MRD positivity (molecular residual disease after curative treatment)","tldr":"A ctDNA MRD test looks for the tumour's own mutations in blood after surgery. Detection predicts relapse months before scans, and in 2026 the FDA approved Signatera as the companion test selecting bladder cancer patients for adjuvant atezolizumab.","route":"/biomarkers/ctdna-mrd-positive/","kind":"biomarker","sub":"Genome-wide readout","facets":{"kind":["Biomarker"],"cancers":["Bladder & urothelial cancer","Colorectal cancer","Triple-negative breast cancer","Non-small-cell lung cancer","Breast cancer","Early triple-negative breast cancer","Pancreatic ductal adenocarcinoma","Resectable pancreatic ductal adenocarcinoma","Diffuse large B-cell lymphoma","Non-Hodgkin lymphoma","Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Bladder & urothelial cancer","href":"/cancers/urothelial/","tip":"Bladder cancer went from 40 years of cisplatin to an ADC-immunotherapy combination that nearly doubled survival, and in 2026 the first blood-test-guided drug approval."},{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."},{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"genome-wide","href":"/tagged/genome-wide/","tip":"Every record tagged genome-wide."},{"label":"ctdna","href":"/tagged/ctdna/","tip":"Every record tagged ctdna."}]},"sortKeys":{"year":0}},{"id":"dll3-expression","name":"DLL3 expression","tldr":"DLL3 sits on the surface of about 85 percent of small-cell lung cancers and almost no normal adult tissue. Tarlatamab is given without a DLL3 test.","route":"/biomarkers/dll3-expression/","kind":"biomarker","target":{"id":"dll3","name":"DLL3","targetClass":"surface-antigen","tldr":"A protein that appears on the surface of small-cell lung cancer cells, now hit by a drug that pulls T cells onto them."},"sub":"DLL3","facets":{"kind":["Biomarker"],"cancers":["Small-cell lung cancer","Extensive-stage small-cell lung cancer","Neuroendocrine and small-cell prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Small-cell lung cancer","href":"/cancers/sclc/","tip":"A fast-growing lung cancer. About a third of cases are confined to one side of the chest and are treated to cure with chemotherapy and radiotherapy together; the rest respond to chemotherapy and relapse quickly. After 30 years without progress, durvalumab consolidation, the T-cell engager tarlatamab and antibody-drug conjugates have each lengthened survival since 2024."},{"label":"Extensive-stage small-cell lung cancer","href":"/cancers/extensive-stage-sclc/","tip":"Small-cell lung cancer that has spread responds fast to chemotherapy but almost always returns within a year. Adding an immunotherapy antibody to first-line chemotherapy helps a minority live for years, and the T-cell engager tarlatamab, which points immune cells at the DLL3 protein on the cancer, has for the first time lengthened life after relapse."},{"label":"Neuroendocrine and small-cell prostate cancer","href":"/cancers/prostate-nepc/","tip":"Neuroendocrine prostate cancer is a form that has stopped depending on the androgen receptor, either from the start or after years of hormone therapy. It no longer shows up on PSA, spreads to the liver and brain, and is treated with the platinum chemotherapy used for small-cell lung cancer."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"dmmr-ihc","name":"dMMR (mismatch repair deficiency by IHC)","tldr":"dMMR means one of the four mismatch repair proteins is missing from the tumour cell nuclei on a stain. It is the tissue-level twin of MSI-high and opens checkpoint immunotherapy in endometrial, bowel and many other cancers.","route":"/biomarkers/dmmr-ihc/","kind":"biomarker","target":{"id":"mmr","name":"Mismatch repair proteins (MLH1, MSH2, MSH6, PMS2)","targetClass":"enzyme","tldr":"The four mismatch repair proteins proofread newly copied DNA; when a tumour loses one of them its DNA fills with small errors, and that state (dMMR or MSI-high) is what lets immunotherapy work across many cancers."},"sub":"MLH1, MSH2, MSH6, PMS2","facets":{"kind":["Biomarker"],"cancers":["Endometrial cancer","Mismatch-repair-deficient endometrial cancer","Colorectal cancer","Microsatellite-unstable (MSI-high) gastric cancer","Metastatic cancer","Triple-negative breast cancer","Pancreatic ductal adenocarcinoma","Mismatch repair deficient (MSI-high) pancreatic ductal adenocarcinoma","Gallbladder cancer","Biliary tract cancer","Prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Endometrial cancer","href":"/cancers/endometrial/","tip":"The gynaecological cancer where immunotherapy has had the biggest impact, guided by molecular classification."},{"label":"Mismatch-repair-deficient endometrial cancer","href":"/cancers/endometrial-mmr-deficient/","tip":"Mismatch-repair-deficient endometrial cancer has lost the machinery that corrects copying errors in DNA, so it accumulates thousands of mutations that make it visible to the immune system. Adding dostarlimab or pembrolizumab to chemotherapy in advanced disease cut the risk of progression by about seventy percent, and many patients remain in remission years later."},{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Microsatellite-unstable (MSI-high) gastric cancer","href":"/cancers/gastric-msi-high/","tip":"Microsatellite-unstable gastric cancer has lost its DNA mismatch repair machinery, carries thousands of mutations and is unusually visible to the immune system. It responds strongly to checkpoint antibodies, may gain little from chemotherapy, and in early-stage disease immunotherapy before surgery is making many tumours disappear entirely."}],"tags":[{"label":"mmr","href":"/tagged/mmr/","tip":"Every record tagged mmr."}]},"sortKeys":{"year":0}},{"id":"myc-bcl2-double-expressor","name":"Double expressor: MYC and BCL2 protein together by immunohistochemistry","tldr":"A stain showing that a lymphoma makes a lot of both the growth protein MYC and the survival protein BCL2, without the genes being rearranged. It predicts a worse course, but on its own it does not change the treatment.","route":"/biomarkers/myc-bcl2-double-expressor/","kind":"biomarker","target":{"id":"myc-gene","name":"MYC","targetClass":"transcription","tldr":"MYC (Myc proto-oncogene protein) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Skin cancer, Multiple myeloma and 5 more."},"sub":"MYC","facets":{"kind":["Biomarker"],"cancers":["Diffuse large B-cell lymphoma","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Diffuse large B-cell lymphoma","href":"/cancers/dlbcl/","tip":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive but curable lymphoma. CAR-T cures about 40% of relapsed patients, and off-the-shelf bispecifics are now approved."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."}],"tags":[{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"double-hit-rearrangement","name":"Double-hit and triple-hit: MYC with BCL2 and BCL6 rearrangement","tldr":"A lymphoma that carries a rearrangement of MYC, the gene that drives growth, together with one of BCL2 or BCL6, the genes that stop a cell dying. Having both is far worse than having either, and it usually means a stronger treatment than standard R-CHOP.","route":"/biomarkers/double-hit-rearrangement/","kind":"biomarker","target":{"id":"myc-gene","name":"MYC","targetClass":"transcription","tldr":"MYC (Myc proto-oncogene protein) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Skin cancer, Multiple myeloma and 5 more."},"sub":"MYC","facets":{"kind":["Biomarker"],"cancers":["Diffuse large B-cell lymphoma","Burkitt lymphoma","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Diffuse large B-cell lymphoma","href":"/cancers/dlbcl/","tip":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive but curable lymphoma. CAR-T cures about 40% of relapsed patients, and off-the-shelf bispecifics are now approved."},{"label":"Burkitt lymphoma","href":"/cancers/burkitt-lymphoma/","tip":"Burkitt lymphoma is the fastest-growing human tumour, driven by a single rearrangement that switches on the MYC gene. That speed makes it exquisitely sensitive to chemotherapy: short, intense courses, now with the antibody rituximab, cure the great majority of children in well-resourced settings. The remaining task is to bring the same cure to the African children who make up most cases."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."}],"tags":[{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"egfr-c797s","name":"EGFR C797S (and its phase with T790M)","tldr":"A change in the EGFR protein that removes the anchor point the newest lung cancer pills grip. Whether it can be worked around depends on whether it sits on the same copy of the gene as the earlier resistance change or on the other copy.","route":"/biomarkers/egfr-c797s/","kind":"biomarker","target":{"id":"egfr","name":"EGFR","targetClass":"kinase","tldr":"A growth receptor that is mutated in some lung cancers and overproduced in others; the first great success of targeted pills."},"sub":"EGFR","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."}]},"sortKeys":{"year":0}},{"id":"egfr-exon-19-deletion","name":"EGFR exon 19 deletion","tldr":"An exon 19 deletion removes a few amino acids from the EGFR kinase and leaves it switched on. With L858R it makes up about 85 percent of EGFR-mutant lung cancer and is the classic gate for osimertinib and the other EGFR inhibitors.","route":"/biomarkers/egfr-exon-19-deletion/","kind":"biomarker","target":{"id":"egfr","name":"EGFR","targetClass":"kinase","tldr":"A growth receptor that is mutated in some lung cancers and overproduced in others; the first great success of targeted pills."},"sub":"EGFR","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"egfr","href":"/tagged/egfr/","tip":"Every record tagged egfr."}]},"sortKeys":{"year":0}},{"id":"egfr-exon-20-insertion","name":"EGFR exon 20 insertion","tldr":"Exon 20 insertions add amino acids after the C-helix of EGFR and make the kinase resistant to the usual EGFR tablets. They account for about a tenth of EGFR mutations and have their own drugs: amivantamab with chemotherapy and sunvozertinib.","route":"/biomarkers/egfr-exon-20-insertion/","kind":"biomarker","target":{"id":"egfr","name":"EGFR","targetClass":"kinase","tldr":"A growth receptor that is mutated in some lung cancers and overproduced in others; the first great success of targeted pills."},"sub":"EGFR","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"egfr","href":"/tagged/egfr/","tip":"Every record tagged egfr."}]},"sortKeys":{"year":0}},{"id":"egfr-l858r","name":"EGFR L858R","tldr":"L858R is a single letter change in exon 21 of EGFR that keeps the kinase active. It is the second commonest sensitising mutation and shares every EGFR inhibitor label with the exon 19 deletion.","route":"/biomarkers/egfr-l858r/","kind":"biomarker","target":{"id":"egfr","name":"EGFR","targetClass":"kinase","tldr":"A growth receptor that is mutated in some lung cancers and overproduced in others; the first great success of targeted pills."},"sub":"EGFR","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"egfr","href":"/tagged/egfr/","tip":"Every record tagged egfr."}]},"sortKeys":{"year":0}},{"id":"egfr-t790m","name":"EGFR T790M","tldr":"T790M is the gatekeeper mutation that lung cancers acquire to escape first- and second-generation EGFR inhibitors. Finding it, in tissue or blood, is the historic gate for osimertinib after an earlier EGFR drug.","route":"/biomarkers/egfr-t790m/","kind":"biomarker","target":{"id":"egfr","name":"EGFR","targetClass":"kinase","tldr":"A growth receptor that is mutated in some lung cancers and overproduced in others; the first great success of targeted pills."},"sub":"EGFR","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"egfr","href":"/tagged/egfr/","tip":"Every record tagged egfr."},{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."}]},"sortKeys":{"year":0}},{"id":"rejuv-age-epigenetic-clocks","name":"Epigenetic age after cancer treatment","tldr":"An epigenetic clock reads chemical marks on DNA and estimates how old the body looks, which is not always the age on a birth certificate. In survivors of childhood cancer the clock runs ahead of chronological age, and the gap is larger after radiotherapy and after certain chemotherapy drugs. What the gap means for any one person is not yet known, and the clocks do not agree with each other.","route":"/technologies/rejuv-age-epigenetic-clocks/","status":"emerging","kind":"technology","schematic":{"id":"rejuv-age-epigenetic-clocks","sections":["rejuvenation","supportive-care"]},"facets":{"kind":["Technology"],"cancers":[],"year":[]},"cols":{"kind":{"facet":"kind","value":"Technology","tip":"Every way we see, measure, or attack a tumour, explained."},"cancers":[],"tags":[{"label":"rejuvenation","href":"/tagged/rejuvenation/","tip":"Every record tagged rejuvenation."},{"label":"survivorship","href":"/tagged/survivorship/","tip":"Every record tagged survivorship."},{"label":"biological-ageing","href":"/tagged/biological-ageing/","tip":"Every record tagged biological-ageing."},{"label":"epigenetics","href":"/tagged/epigenetics/","tip":"Every record tagged epigenetics."}]},"sortKeys":{"year":0}},{"id":"er-status","name":"ER status (oestrogen receptor by IHC)","tldr":"ER status is whether the tumour's cells carry the oestrogen receptor, read by staining nuclei. One percent or more of stained nuclei is positive and means hormone-blocking treatment can work; 1 to 10 percent is 'low positive' and behaves more like negative.","route":"/biomarkers/er-status/","kind":"biomarker","target":{"id":"estrogen-receptor","name":"Estrogen receptor (ERα)","targetClass":"nuclear-receptor","tldr":"The hormone switch that drives most breast cancers. Blocking or destroying it is the oldest and most effective targeted therapy."},"sub":"ESR1","facets":{"kind":["Biomarker"],"cancers":["HR-positive / HER2-negative breast cancer","Breast cancer","High-risk early HR-positive breast cancer","HR-positive metastatic breast cancer after CDK4/6 inhibitors","Endometrial cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Breast cancer","href":"/cancers/breast-cancer/","tip":"Breast cancer is not one disease, and the result that decides which page you need is the receptor result: whether the cancer carries oestrogen and progesterone receptors, and whether it carries too much HER2. Those two answers give four boxes, not three, with a page for each. Grade and stage do not change which page you read; they change what happens on it."},{"label":"High-risk early HR-positive breast cancer","href":"/cancers/hr-positive-early-high-risk/","tip":"Most hormone-driven breast cancers are cured with surgery, radiotherapy and five to ten years of endocrine tablets. Women whose tumours are larger, higher grade or have reached the lymph nodes face a higher risk of relapse: two to three years of a CDK4/6 inhibitor added to endocrine therapy cuts recurrence, and genomic tests such as Oncotype DX and MammaPrint decide who also needs chemotherapy."},{"label":"HR-positive metastatic breast cancer after CDK4/6 inhibitors","href":"/cancers/hr-positive-metastatic-post-cdk46/","tip":"When hormone-positive breast cancer grows through a CDK4/6 inhibitor, a blood test picks the next drug. Tumours with an acquired ESR1 mutation respond to the oral degraders elacestrant, camizestrant and imlunestrant; tumours with PIK3CA, AKT1 or PTEN changes to capivasertib, inavolisib or alpelisib; and once endocrine options run out, antibody-drug conjugates come before chemotherapy."}],"tags":[{"label":"hormone-receptor","href":"/tagged/hormone-receptor/","tip":"Every record tagged hormone-receptor."}]},"sortKeys":{"year":0}},{"id":"esr1-mutation-ctdna","name":"ESR1 mutation (ligand-binding domain, usually in ctDNA)","tldr":"ESR1 mutations arise in the oestrogen receptor's ligand-binding domain after aromatase inhibitor treatment, letting the receptor work without oestrogen. They are usually found in a blood test and select the oral SERDs elacestrant and imlunestrant.","route":"/biomarkers/esr1-mutation-ctdna/","kind":"biomarker","target":{"id":"estrogen-receptor","name":"Estrogen receptor (ERα)","targetClass":"nuclear-receptor","tldr":"The hormone switch that drives most breast cancers. Blocking or destroying it is the oldest and most effective targeted therapy."},"sub":"ESR1","facets":{"kind":["Biomarker"],"cancers":["HR-positive / HER2-negative breast cancer","HR-positive metastatic breast cancer after CDK4/6 inhibitors"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"HR-positive metastatic breast cancer after CDK4/6 inhibitors","href":"/cancers/hr-positive-metastatic-post-cdk46/","tip":"When hormone-positive breast cancer grows through a CDK4/6 inhibitor, a blood test picks the next drug. Tumours with an acquired ESR1 mutation respond to the oral degraders elacestrant, camizestrant and imlunestrant; tumours with PIK3CA, AKT1 or PTEN changes to capivasertib, inavolisib or alpelisib; and once endocrine options run out, antibody-drug conjugates come before chemotherapy."}],"tags":[{"label":"hormone-receptor","href":"/tagged/hormone-receptor/","tip":"Every record tagged hormone-receptor."},{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."}]},"sortKeys":{"year":0}},{"id":"ezh2-y646-mutation","name":"EZH2 gain-of-function mutation (Tyr646, originally Tyr641)","tldr":"A change in an enzyme that puts a chemical silencing mark on DNA. The altered enzyme adds too much of the mark, which keeps a lymphoma cell locked in the state it should have grown out of. It is the one lymphoma mutation that currently selects a tablet.","route":"/biomarkers/ezh2-y646-mutation/","kind":"biomarker","target":{"id":"ezh2","name":"EZH2","targetClass":"enzyme","tldr":"EZH2 is an enzyme that silences genes. The first drug against it treated a rare sarcoma and some lymphomas until it was withdrawn in 2026 for causing second blood cancers."},"sub":"EZH2","facets":{"kind":["Biomarker"],"cancers":["Follicular lymphoma","Diffuse large B-cell lymphoma","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Follicular lymphoma","href":"/cancers/follicular-lymphoma/","tip":"Follicular lymphoma is the most common slow-growing lymphoma, defined in about 85% of cases by a BCL2 translocation. Most people live with it for decades, treated only when it causes problems; it can be controlled repeatedly with anti-CD20 antibodies, chemotherapy, bispecifics or CAR-T but rarely cured, and a small share transform into an aggressive lymphoma each year."},{"label":"Diffuse large B-cell lymphoma","href":"/cancers/dlbcl/","tip":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive but curable lymphoma. CAR-T cures about 40% of relapsed patients, and off-the-shelf bispecifics are now approved."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."}],"tags":[{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"fcrh5-expression","name":"FcRH5 expression","tldr":"FcRH5 is a third myeloma surface target after BCMA and GPRC5D. Cevostamab, the FcRH5 x CD3 bispecific, is in phase 3; no approval or threshold exists yet.","route":"/biomarkers/fcrh5-expression/","kind":"biomarker","target":{"id":"fcrh5","name":"FcRH5 (FCRL5)","targetClass":"surface-antigen","tldr":"FcRH5 is a surface protein found almost only on B cells and myeloma plasma cells, which makes it a target for T-cell engaging antibodies in multiple myeloma."},"sub":"FCRL5","facets":{"kind":["Biomarker"],"cancers":["Multiple myeloma","Relapsed or refractory multiple myeloma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Multiple myeloma","href":"/cancers/multiple-myeloma/","tip":"Multiple myeloma is a plasma-cell cancer with more new drug classes than any other: proteasome inhibitors, IMiDs, CD38 antibodies, BCMA CAR-T, bispecifics, and an ADC."},{"label":"Relapsed or refractory multiple myeloma","href":"/cancers/myeloma-relapsed-refractory/","tip":"Myeloma almost always returns, and each return is harder to treat. Two kinds of immune therapy aimed at the BCMA protein on myeloma cells, CAR-T cells (KarMMa-3, CARTITUDE-4) and off-the-shelf bispecific antibodies (MajesTEC), now give deep remissions after other drugs fail, and a second target, GPRC5D, gives another option."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"fgfr2-fusion-rearrangement","name":"FGFR2 fusion or rearrangement","tldr":"FGFR2 fusions occur in 10 to 15 percent of intrahepatic bile duct cancers and almost nowhere else. Pemigatinib and futibatinib are approved for them after a first chemotherapy.","route":"/biomarkers/fgfr2-fusion-rearrangement/","kind":"biomarker","target":{"id":"fgfr2","name":"FGFR2","targetClass":"kinase","tldr":"FGFR2 is a growth receptor fused in bile-duct cancer and overproduced in gastric cancer."},"sub":"FGFR2","facets":{"kind":["Biomarker"],"cancers":["Biliary tract cancer","Intrahepatic cholangiocarcinoma","Biliary tract cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Biliary tract cancer","href":"/cancers/cholangiocarcinoma/","tip":"Cholangiocarcinoma is cancer of the bile ducts or gallbladder. It is rare and often found late, but it turned out to carry more targetable mutations than almost any other gastrointestinal cancer, and immunotherapy now adds to chemotherapy from the first treatment."},{"label":"Intrahepatic cholangiocarcinoma","href":"/cancers/intrahepatic-cholangiocarcinoma/","tip":"Intrahepatic cholangiocarcinoma starts in the small bile ducts inside the liver and usually appears as a liver mass rather than causing jaundice. It is the biliary cancer with the most drug targets: FGFR2 fusions treated with pemigatinib or futibatinib, IDH1 mutations with ivosidenib, and for everyone chemotherapy with the immunotherapy durvalumab or pembrolizumab."},{"label":"Biliary tract cancer","href":"/cancers/biliary-tract-cancer/","tip":"Biliary tract cancers arise in the bile ducts inside or outside the liver, the gallbladder or the ampulla where the duct meets the bowel. They share short survival and the same first-line chemotherapy with immunotherapy, but differ in causes and in the targetable mutations they carry. Each has its own page."}],"tags":[{"label":"fgfr","href":"/tagged/fgfr/","tip":"Every record tagged fgfr."}]},"sortKeys":{"year":0}},{"id":"fgfr3-alteration","name":"FGFR3 alteration (mutation or fusion)","tldr":"FGFR3 point mutations and TACC3 fusions drive about 15 to 20 percent of advanced bladder cancers. Erdafitinib is approved for tumours with these 'susceptible' alterations after one prior treatment.","route":"/biomarkers/fgfr3-alteration/","kind":"biomarker","target":{"id":"fgfr3-receptor","name":"FGFR3","targetClass":"kinase","tldr":"A growth-factor receptor that is mutated or fused in a sizeable minority of bladder cancers. Erdafitinib blocks it and is the first targeted drug approved for urothelial cancer selected by a genomic test."},"sub":"FGFR3","facets":{"kind":["Biomarker"],"cancers":["Bladder & urothelial cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Bladder & urothelial cancer","href":"/cancers/urothelial/","tip":"Bladder cancer went from 40 years of cisplatin to an ADC-immunotherapy combination that nearly doubled survival, and in 2026 the first blood-test-guided drug approval."}],"tags":[{"label":"fgfr","href":"/tagged/fgfr/","tip":"Every record tagged fgfr."}]},"sortKeys":{"year":0}},{"id":"flt3-itd","name":"FLT3-ITD (internal tandem duplication)","tldr":"FLT3-ITD is a duplicated stretch of the FLT3 receptor gene found in about a quarter of acute myeloid leukaemias; it makes relapse more likely and is treated with midostaurin, quizartinib or gilteritinib.","route":"/biomarkers/flt3-itd/","kind":"biomarker","target":{"id":"flt3","name":"FLT3","targetClass":"kinase","tldr":"FLT3 is a kinase mutated in about a third of acute myeloid leukaemias, where adding an inhibitor to chemotherapy improves survival."},"sub":"FLT3","facets":{"kind":["Biomarker"],"cancers":["Acute myeloid leukaemia","FLT3-mutated acute myeloid leukaemia"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"FLT3-mutated acute myeloid leukaemia","href":"/cancers/aml-flt3/","tip":"FLT3-mutated acute myeloid leukaemia carries a mutation in a growth-signal receptor that makes the leukaemia relapse quickly. Adding a FLT3 blocker to chemotherapy, midostaurin or quizartinib, lengthens life, and gilteritinib is the standard when the disease comes back."}],"tags":[{"label":"flt3","href":"/tagged/flt3/","tip":"Every record tagged flt3."}]},"sortKeys":{"year":0}},{"id":"flt3-tkd","name":"FLT3-TKD (D835 and I836 tyrosine kinase domain mutations)","tldr":"FLT3-TKD mutations are point changes in the kinase's activation loop, found in about 7 percent of acute myeloid leukaemias. Midostaurin and gilteritinib labels cover them; quizartinib's does not.","route":"/biomarkers/flt3-tkd/","kind":"biomarker","target":{"id":"flt3","name":"FLT3","targetClass":"kinase","tldr":"FLT3 is a kinase mutated in about a third of acute myeloid leukaemias, where adding an inhibitor to chemotherapy improves survival."},"sub":"FLT3","facets":{"kind":["Biomarker"],"cancers":["Acute myeloid leukaemia","FLT3-mutated acute myeloid leukaemia"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"FLT3-mutated acute myeloid leukaemia","href":"/cancers/aml-flt3/","tip":"FLT3-mutated acute myeloid leukaemia carries a mutation in a growth-signal receptor that makes the leukaemia relapse quickly. Adding a FLT3 blocker to chemotherapy, midostaurin or quizartinib, lengthens life, and gilteritinib is the standard when the disease comes back."}],"tags":[{"label":"flt3","href":"/tagged/flt3/","tip":"Every record tagged flt3."}]},"sortKeys":{"year":0}},{"id":"folr1-expression","name":"Folate receptor alpha expression (FRα-positive, PS2+ >= 75%)","tldr":"Folate receptor alpha is a surface protein on most high-grade serous ovarian cancers. Mirvetuximab soravtansine requires FRα-positive disease, scored as at least 75 percent of cells with moderate or strong staining on the Ventana FOLR1 assay.","route":"/biomarkers/folr1-expression/","kind":"biomarker","target":{"id":"folr1","name":"Folate receptor alpha","targetClass":"surface-antigen","tldr":"Folate receptor alpha is a vitamin receptor that ovarian cancer cells carry in large numbers, used as the docking site for the ADC mirvetuximab."},"sub":"FOLR1","facets":{"kind":["Biomarker"],"cancers":["Ovarian cancer","Platinum-resistant ovarian cancer","High-grade serous ovarian cancer","Endometrial cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Ovarian cancer","href":"/cancers/ovarian/","tip":"Usually found late. PARP inhibitors transformed maintenance therapy, and ADCs against folate receptor and CDH6 are arriving for platinum-resistant disease."},{"label":"Platinum-resistant ovarian cancer","href":"/cancers/platinum-resistant-ovarian-cancer/","tip":"Platinum-resistant ovarian cancer grows back within six months of platinum chemotherapy, or during it, and used to be treated with single chemotherapy drugs that shrink a tumour one time in ten. The antibody-drug conjugate mirvetuximab soravtansine, the cortisol-blocking drug relacorilant and pembrolizumab in PD-L1-positive tumours have each extended survival in phase 3 trials since 2023."},{"label":"High-grade serous ovarian cancer","href":"/cancers/high-grade-serous-ovarian-cancer/","tip":"High-grade serous cancer is the common, aggressive form of ovarian cancer, now known to start in the fallopian tube. It is treated with surgery and platinum chemotherapy, and maintenance PARP inhibitors have changed its course for the half of patients whose tumours cannot repair DNA properly."},{"label":"Endometrial cancer","href":"/cancers/endometrial/","tip":"The gynaecological cancer where immunotherapy has had the biggest impact, guided by molecular classification."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."}]},"sortKeys":{"year":0}},{"id":"rejuv-second-from-clone-to-disease","name":"From a clone in the blood to a leukaemia: what is known, and what is done","tldr":"Chemotherapy and radiotherapy select for blood stem cells carrying particular mutations, and in a small minority one of those clones becomes a leukaemia. The useful question is not whether a clone is there but whether it will progress: most never do, and nothing has been shown to stop one that does.","route":"/terms/rejuv-second-from-clone-to-disease/","kind":"term","schematic":{"id":"wes-wgs","sections":["diagnostics","drug-discovery"]},"facets":{"kind":["Term"],"cancers":["Acute myeloid leukaemia","Myelodysplastic syndromes / neoplasms","Secondary and therapy-related acute myeloid leukaemia","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Term","tip":"Glossary with plain-English TL;DRs and Wikipedia links."},"cancers":[{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"Myelodysplastic syndromes / neoplasms","href":"/cancers/mds/","tip":"Bone-marrow disorders where blood cells are made badly and too few reach the blood; a third progress to acute leukaemia. Treatment ranges from transfusions and growth factors to hypomethylating drugs and, for the fit, transplant."},{"label":"Secondary and therapy-related acute myeloid leukaemia","href":"/cancers/aml-secondary/","tip":"Secondary acute myeloid leukaemia grows out of an earlier marrow disorder or follows chemotherapy or radiotherapy for another cancer. It resists standard treatment more than other leukaemias; a liposomal form of the two classic chemotherapy drugs, CPX-351, lengthens life in fit older patients, and transplant is the only route to cure."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."}],"tags":[{"label":"rejuvenation","href":"/tagged/rejuvenation/","tip":"Every record tagged rejuvenation."},{"label":"survivorship","href":"/tagged/survivorship/","tip":"Every record tagged survivorship."},{"label":"second-cancers","href":"/tagged/second-cancers/","tip":"Every record tagged second-cancers."},{"label":"blood","href":"/tagged/blood/","tip":"Every record tagged blood."}]},"sortKeys":{"year":0}},{"id":"brca-germline","name":"Germline BRCA1/2 pathogenic variant (gBRCAm)","tldr":"A germline BRCA1 or BRCA2 variant is inherited and present in every cell, found by a blood test. It selects PARP inhibitors in breast, ovarian, pancreatic and prostate cancer and tells relatives they may carry it too.","route":"/biomarkers/brca-germline/","kind":"biomarker","target":{"id":"brca","name":"BRCA1 / BRCA2 (HRD)","targetClass":"tumor-suppressor","tldr":"DNA repair genes. Inheriting a broken copy raises breast and ovarian cancer risk, but tumours that lose them become uniquely vulnerable to PARP inhibitors and platinum."},"sub":"BRCA1, BRCA2","facets":{"kind":["Biomarker"],"cancers":["Breast cancer","Triple-negative breast cancer","HR-positive / HER2-negative breast cancer","Ovarian cancer","High-grade serous ovarian cancer","Pancreatic ductal adenocarcinoma","Metastatic castration-resistant prostate cancer","Early triple-negative breast cancer","Metastatic triple-negative breast cancer","BRCA or PALB2-mutant pancreatic ductal adenocarcinoma","Metastatic pancreatic ductal adenocarcinoma","Prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Breast cancer","href":"/cancers/breast-cancer/","tip":"Breast cancer is not one disease, and the result that decides which page you need is the receptor result: whether the cancer carries oestrogen and progesterone receptors, and whether it carries too much HER2. Those two answers give four boxes, not three, with a page for each. Grade and stage do not change which page you read; they change what happens on it."},{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."},{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Ovarian cancer","href":"/cancers/ovarian/","tip":"Usually found late. PARP inhibitors transformed maintenance therapy, and ADCs against folate receptor and CDH6 are arriving for platinum-resistant disease."}],"tags":[{"label":"brca","href":"/tagged/brca/","tip":"Every record tagged brca."}]},"sortKeys":{"year":0}},{"id":"gprc5d-expression","name":"GPRC5D expression","tldr":"GPRC5D is a receptor on myeloma cells and in hair follicles, nails and taste buds. Talquetamab targets it without any test, and the side effects on skin, nails and taste follow from where it is expressed.","route":"/biomarkers/gprc5d-expression/","kind":"biomarker","target":{"id":"gprc5d","name":"GPRC5D","targetClass":"surface-antigen","tldr":"GPRC5D is a second myeloma target used when BCMA-directed drugs stop working."},"sub":"GPRC5D","facets":{"kind":["Biomarker"],"cancers":["Multiple myeloma","Relapsed or refractory multiple myeloma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Multiple myeloma","href":"/cancers/multiple-myeloma/","tip":"Multiple myeloma is a plasma-cell cancer with more new drug classes than any other: proteasome inhibitors, IMiDs, CD38 antibodies, BCMA CAR-T, bispecifics, and an ADC."},{"label":"Relapsed or refractory multiple myeloma","href":"/cancers/myeloma-relapsed-refractory/","tip":"Myeloma almost always returns, and each return is harder to treat. Two kinds of immune therapy aimed at the BCMA protein on myeloma cells, CAR-T cells (KarMMa-3, CARTITUDE-4) and off-the-shelf bispecific antibodies (MajesTEC), now give deep remissions after other drugs fail, and a second target, GPRC5D, gives another option."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"h3-k27m","name":"H3 K27M mutation","tldr":"H3 K27M is a single change in a histone that defines diffuse midline glioma, including the brain-stem tumour DIPG. In 2025 dordaviprone became the first drug approved for tumours carrying it.","route":"/biomarkers/h3-k27m/","kind":"biomarker","target":{"id":"h3-3a","name":"Histone H3.3 (H3-3A)","targetClass":"other","tldr":"H3.3 is one of the histone proteins DNA wraps around; a single change at position 27 (K27M) locks brain-stem and midline gliomas in an immature state and defines the diagnosis."},"sub":"H3-3A","facets":{"kind":["Biomarker"],"cancers":["Diffuse midline glioma, H3 K27-altered","Paediatric high-grade glioma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Diffuse midline glioma, H3 K27-altered","href":"/cancers/dipg-dmg/","tip":"Diffuse midline glioma grows through the brainstem and cannot be removed surgically. A single change in a histone protein (H3 K27M) rewires how the tumour reads its DNA. Radiotherapy was long the only help; in 2025 the first drug aimed at this tumour, dordaviprone (ONC201), was approved after durable shrinkage in some patients, and GD2 CAR-T cells have produced striking early responses."},{"label":"Paediatric high-grade glioma","href":"/cancers/paediatric-high-grade-glioma/","tip":"High-grade gliomas in children look like adult glioblastoma under the microscope but are driven by different genes, so they are now classified separately. Surgery and radiotherapy remain the mainstay and chemotherapy adds little; the real gains are in small subsets with a targetable gene change, such as BRAF V600E tumours and the fusion-driven tumours of infants."}],"tags":[{"label":"glioma","href":"/tagged/glioma/","tip":"Every record tagged glioma."},{"label":"paediatric","href":"/tagged/paediatric/","tip":"Every record tagged paediatric."}]},"sortKeys":{"year":0}},{"id":"her2-mutation","name":"HER2 (ERBB2) activating mutation","tldr":"A HER2 mutation is a change in the gene's kinase domain, most often an exon 20 insertion, found in about 2 to 3 percent of lung adenocarcinomas. It is a different thing from HER2 amplification or overexpression, and it selects trastuzumab deruxtecan and, since 2025, zongertinib in lung cancer.","route":"/biomarkers/her2-mutation/","kind":"biomarker","target":{"id":"her2","name":"HER2","targetClass":"surface-antigen","tldr":"A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers."},"sub":"ERBB2","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Gallbladder cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Gallbladder cancer","href":"/cancers/gallbladder/","tip":"Gallbladder cancer starts in the small bile-storing sac under the liver and is one of the biliary tract cancers. Most cases are found late, or by chance when a gallbladder is removed for gallstones. It is rare in the UK, with about 1,300 cases a year, and much commoner in Chile, Bolivia and northern India. Found early, an operation can cure it."}],"tags":[{"label":"her2","href":"/tagged/her2/","tip":"Every record tagged her2."}]},"sortKeys":{"year":0}},{"id":"her2-ihc-0","name":"HER2 IHC 0 (HER2-negative, including ultralow)","tldr":"IHC 0 is no HER2 staining, or faint staining in 10 percent or fewer cells. It is HER2-negative, but the label now separates true zero from 'IHC 0 with membrane staining', the ultralow group that trastuzumab deruxtecan can treat in hormone-receptor-positive breast cancer.","route":"/biomarkers/her2-ihc-0/","kind":"biomarker","target":{"id":"her2","name":"HER2","targetClass":"surface-antigen","tldr":"A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers."},"sub":"ERBB2","facets":{"kind":["Biomarker"],"cancers":["Breast cancer","HER2-low and HER2-ultralow metastatic breast cancer","HR-positive / HER2-negative breast cancer","Triple-negative breast cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Breast cancer","href":"/cancers/breast-cancer/","tip":"Breast cancer is not one disease, and the result that decides which page you need is the receptor result: whether the cancer carries oestrogen and progesterone receptors, and whether it carries too much HER2. Those two answers give four boxes, not three, with a page for each. Grade and stage do not change which page you read; they change what happens on it."},{"label":"HER2-low and HER2-ultralow metastatic breast cancer","href":"/cancers/her2-low-metastatic-breast-cancer/","tip":"HER2-low is not a new kind of breast cancer but a new way of reading an old test: tumours once called HER2-negative that carry a little HER2 protein. That trace is enough for the antibody-drug conjugate trastuzumab deruxtecan to deliver its chemotherapy payload, and since 2022 it has been the standard for these patients after endocrine therapy or a first chemotherapy."},{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."}],"tags":[{"label":"her2","href":"/tagged/her2/","tip":"Every record tagged her2."}]},"sortKeys":{"year":0}},{"id":"her2-ihc-1-plus","name":"HER2 IHC 1+","tldr":"IHC 1+ is faint, incomplete HER2 staining. It was called HER2-negative for twenty years; since 2022 it is the larger half of HER2-low, which trastuzumab deruxtecan treats in breast cancer.","route":"/biomarkers/her2-ihc-1-plus/","kind":"biomarker","target":{"id":"her2","name":"HER2","targetClass":"surface-antigen","tldr":"A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers."},"sub":"ERBB2","facets":{"kind":["Biomarker"],"cancers":["Breast cancer","HER2-low and HER2-ultralow metastatic breast cancer","HR-positive / HER2-negative breast cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Breast cancer","href":"/cancers/breast-cancer/","tip":"Breast cancer is not one disease, and the result that decides which page you need is the receptor result: whether the cancer carries oestrogen and progesterone receptors, and whether it carries too much HER2. Those two answers give four boxes, not three, with a page for each. Grade and stage do not change which page you read; they change what happens on it."},{"label":"HER2-low and HER2-ultralow metastatic breast cancer","href":"/cancers/her2-low-metastatic-breast-cancer/","tip":"HER2-low is not a new kind of breast cancer but a new way of reading an old test: tumours once called HER2-negative that carry a little HER2 protein. That trace is enough for the antibody-drug conjugate trastuzumab deruxtecan to deliver its chemotherapy payload, and since 2022 it has been the standard for these patients after endocrine therapy or a first chemotherapy."},{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."}],"tags":[{"label":"her2","href":"/tagged/her2/","tip":"Every record tagged her2."}]},"sortKeys":{"year":0}},{"id":"her2-ihc-2-plus","name":"HER2 IHC 2+ (equivocal, reflex to ISH)","tldr":"IHC 2+ is the in-between HER2 result: moderate staining that cannot be called positive or negative by eye, so the laboratory runs an ISH gene test. 2+ with amplification is HER2-positive; 2+ without it is HER2-low.","route":"/biomarkers/her2-ihc-2-plus/","kind":"biomarker","target":{"id":"her2","name":"HER2","targetClass":"surface-antigen","tldr":"A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers."},"sub":"ERBB2","facets":{"kind":["Biomarker"],"cancers":["Breast cancer","HER2-low and HER2-ultralow metastatic breast cancer","HER2-positive gastric cancer","Gallbladder cancer","Biliary tract cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Breast cancer","href":"/cancers/breast-cancer/","tip":"Breast cancer is not one disease, and the result that decides which page you need is the receptor result: whether the cancer carries oestrogen and progesterone receptors, and whether it carries too much HER2. Those two answers give four boxes, not three, with a page for each. Grade and stage do not change which page you read; they change what happens on it."},{"label":"HER2-low and HER2-ultralow metastatic breast cancer","href":"/cancers/her2-low-metastatic-breast-cancer/","tip":"HER2-low is not a new kind of breast cancer but a new way of reading an old test: tumours once called HER2-negative that carry a little HER2 protein. That trace is enough for the antibody-drug conjugate trastuzumab deruxtecan to deliver its chemotherapy payload, and since 2022 it has been the standard for these patients after endocrine therapy or a first chemotherapy."},{"label":"HER2-positive gastric cancer","href":"/cancers/gastric-her2-positive/","tip":"HER2-positive gastric cancer overexpresses the HER2 growth receptor and is treated with trastuzumab added to chemotherapy, now usually with pembrolizumab as well. After progression the antibody-drug conjugate trastuzumab deruxtecan gives responses that plain chemotherapy cannot."},{"label":"Gallbladder cancer","href":"/cancers/gallbladder/","tip":"Gallbladder cancer starts in the small bile-storing sac under the liver and is one of the biliary tract cancers. Most cases are found late, or by chance when a gallbladder is removed for gallstones. It is rare in the UK, with about 1,300 cases a year, and much commoner in Chile, Bolivia and northern India. Found early, an operation can cure it."}],"tags":[{"label":"her2","href":"/tagged/her2/","tip":"Every record tagged her2."}]},"sortKeys":{"year":0}},{"id":"her2-ihc-3-plus","name":"HER2 IHC 3+ (HER2-positive by immunohistochemistry)","tldr":"IHC 3+ means strong, complete membrane staining for HER2 in more than 10 percent of tumour cells. It is HER2-positive without needing a gene test and is the gate for trastuzumab, its combinations and antibody-drug conjugates in breast, stomach, biliary and, since 2024, any solid tumour.","route":"/biomarkers/her2-ihc-3-plus/","kind":"biomarker","target":{"id":"her2","name":"HER2","targetClass":"surface-antigen","tldr":"A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers."},"sub":"ERBB2","facets":{"kind":["Biomarker"],"cancers":["HER2-positive breast cancer","Early HER2-positive breast cancer","HER2-positive gastric cancer","Biliary tract cancer","Metastatic cancer","Colorectal cancer","Gallbladder cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HER2-positive breast cancer","href":"/cancers/breast-her2-positive/","tip":"HER2-positive breast cancer was once the most aggressive subtype and is now one of the most treatable, thanks to trastuzumab and, more recently, Enhertu."},{"label":"Early HER2-positive breast cancer","href":"/cancers/her2-positive-early-breast-cancer/","tip":"HER2-positive breast cancer caught early is usually cured. Chemotherapy with the antibodies trastuzumab and pertuzumab comes before surgery; if the tumour has gone by then, antibodies alone finish the year, and if cancer remains, trastuzumab emtansine or trastuzumab deruxtecan take over. Small tumours get a gentler regimen, and trials now ask how much treatment can be left out."},{"label":"HER2-positive gastric cancer","href":"/cancers/gastric-her2-positive/","tip":"HER2-positive gastric cancer overexpresses the HER2 growth receptor and is treated with trastuzumab added to chemotherapy, now usually with pembrolizumab as well. After progression the antibody-drug conjugate trastuzumab deruxtecan gives responses that plain chemotherapy cannot."},{"label":"Biliary tract cancer","href":"/cancers/biliary-tract-cancer/","tip":"Biliary tract cancers arise in the bile ducts inside or outside the liver, the gallbladder or the ampulla where the duct meets the bowel. They share short survival and the same first-line chemotherapy with immunotherapy, but differ in causes and in the targetable mutations they carry. Each has its own page."}],"tags":[{"label":"her2","href":"/tagged/her2/","tip":"Every record tagged her2."}]},"sortKeys":{"year":0}},{"id":"her2-ish-amplified","name":"HER2 ISH amplified (ERBB2 gene amplification)","tldr":"ISH counts copies of the HER2 gene in each tumour cell. A ratio of 2 or more against the chromosome 17 control, or 6 or more copies per cell, is amplified and HER2-positive whatever the protein stain showed.","route":"/biomarkers/her2-ish-amplified/","kind":"biomarker","target":{"id":"her2","name":"HER2","targetClass":"surface-antigen","tldr":"A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers."},"sub":"ERBB2","facets":{"kind":["Biomarker"],"cancers":["HER2-positive breast cancer","HER2-positive gastric cancer","Early HER2-positive breast cancer","Colorectal cancer","Gallbladder cancer","Biliary tract cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HER2-positive breast cancer","href":"/cancers/breast-her2-positive/","tip":"HER2-positive breast cancer was once the most aggressive subtype and is now one of the most treatable, thanks to trastuzumab and, more recently, Enhertu."},{"label":"HER2-positive gastric cancer","href":"/cancers/gastric-her2-positive/","tip":"HER2-positive gastric cancer overexpresses the HER2 growth receptor and is treated with trastuzumab added to chemotherapy, now usually with pembrolizumab as well. After progression the antibody-drug conjugate trastuzumab deruxtecan gives responses that plain chemotherapy cannot."},{"label":"Early HER2-positive breast cancer","href":"/cancers/her2-positive-early-breast-cancer/","tip":"HER2-positive breast cancer caught early is usually cured. Chemotherapy with the antibodies trastuzumab and pertuzumab comes before surgery; if the tumour has gone by then, antibodies alone finish the year, and if cancer remains, trastuzumab emtansine or trastuzumab deruxtecan take over. Small tumours get a gentler regimen, and trials now ask how much treatment can be left out."},{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."}],"tags":[{"label":"her2","href":"/tagged/her2/","tip":"Every record tagged her2."}]},"sortKeys":{"year":0}},{"id":"her2-low-ihc","name":"HER2-low (IHC 1+ or IHC 2+/ISH-negative)","tldr":"HER2-low is not a new stain but a new reading of the old one: 1+ or 2+ without gene amplification. It covers about half of breast cancers and makes them eligible for trastuzumab deruxtecan.","route":"/biomarkers/her2-low-ihc/","kind":"biomarker","target":{"id":"her2","name":"HER2","targetClass":"surface-antigen","tldr":"A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers."},"sub":"ERBB2","facets":{"kind":["Biomarker"],"cancers":["HER2-low and HER2-ultralow metastatic breast cancer","HR-positive / HER2-negative breast cancer","Metastatic triple-negative breast cancer","Breast cancer","Triple-negative breast cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HER2-low and HER2-ultralow metastatic breast cancer","href":"/cancers/her2-low-metastatic-breast-cancer/","tip":"HER2-low is not a new kind of breast cancer but a new way of reading an old test: tumours once called HER2-negative that carry a little HER2 protein. That trace is enough for the antibody-drug conjugate trastuzumab deruxtecan to deliver its chemotherapy payload, and since 2022 it has been the standard for these patients after endocrine therapy or a first chemotherapy."},{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Metastatic triple-negative breast cancer","href":"/cancers/tnbc-metastatic/","tip":"The treatment of triple-negative breast cancer that has spread has been transformed since 2020, though it is not yet curable. By PD-L1 score, first treatment is pembrolizumab with chemotherapy or with sacituzumab govitecan, or datopotamab deruxtecan or sacituzumab govitecan alone; BRCA carriers can take a PARP inhibitor tablet; and trastuzumab deruxtecan reaches the third of tumours with low HER2."},{"label":"Breast cancer","href":"/cancers/breast-cancer/","tip":"Breast cancer is not one disease, and the result that decides which page you need is the receptor result: whether the cancer carries oestrogen and progesterone receptors, and whether it carries too much HER2. Those two answers give four boxes, not three, with a page for each. Grade and stage do not change which page you read; they change what happens on it."}],"tags":[{"label":"her2","href":"/tagged/her2/","tip":"Every record tagged her2."}]},"sortKeys":{"year":0}},{"id":"her2-ultralow","name":"HER2-ultralow (IHC 0 with membrane staining)","tldr":"HER2-ultralow is an IHC 0 result with a trace of membrane staining in a few cells. Since 2025, in hormone-receptor-positive breast cancer that has stopped responding to hormone therapy, it is enough for trastuzumab deruxtecan.","route":"/biomarkers/her2-ultralow/","kind":"biomarker","target":{"id":"her2","name":"HER2","targetClass":"surface-antigen","tldr":"A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers."},"sub":"ERBB2","facets":{"kind":["Biomarker"],"cancers":["HER2-low and HER2-ultralow metastatic breast cancer","HR-positive / HER2-negative breast cancer","Triple-negative breast cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HER2-low and HER2-ultralow metastatic breast cancer","href":"/cancers/her2-low-metastatic-breast-cancer/","tip":"HER2-low is not a new kind of breast cancer but a new way of reading an old test: tumours once called HER2-negative that carry a little HER2 protein. That trace is enough for the antibody-drug conjugate trastuzumab deruxtecan to deliver its chemotherapy payload, and since 2022 it has been the standard for these patients after endocrine therapy or a first chemotherapy."},{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."}],"tags":[{"label":"her2","href":"/tagged/her2/","tip":"Every record tagged her2."}]},"sortKeys":{"year":0}},{"id":"her3-expression","name":"HER3 expression","tldr":"HER3 is a signalling partner of EGFR and HER2 present on most lung and breast cancers. Patritumab deruxtecan was studied in EGFR-mutant lung cancer without a HER3 threshold, and no approval exists.","route":"/biomarkers/her3-expression/","kind":"biomarker","target":{"id":"her3","name":"HER3","targetClass":"surface-antigen","tldr":"HER3 is a cousin of HER2 that cancers use as an escape route when HER2 or EGFR are blocked."},"sub":"ERBB3","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Breast cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Breast cancer","href":"/cancers/breast-cancer/","tip":"Breast cancer is not one disease, and the result that decides which page you need is the receptor result: whether the cancer carries oestrogen and progesterone receptors, and whether it carries too much HER2. Those two answers give four boxes, not three, with a page for each. Grade and stage do not change which page you read; they change what happens on it."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"hla-a-02-01","name":"HLA-A*02:01 (HLA typing for TCR therapies)","tldr":"HLA-A*02:01 is the commonest tissue-type molecule in people of European descent and the one the first T-cell receptor therapies were built for. Tebentafusp and afamitresgene autoleucel work only in patients who carry it, so a blood HLA test comes before the tumour test.","route":"/biomarkers/hla-a-02-01/","kind":"biomarker","target":{"id":"hla-a","name":"HLA-A","targetClass":"surface-antigen","tldr":"HLA-A is the molecule that holds up short pieces of a cell's proteins for T cells to inspect. Engineered T-cell receptor therapies such as tebentafusp and afami-cel only work in people with the HLA-A*02 variant, because the receptor recognises the tumour peptide sitting in that particular groove."},"sub":"HLA-A","facets":{"kind":["Biomarker"],"cancers":["Uveal melanoma","Synovial sarcoma","Melanoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Uveal melanoma","href":"/cancers/uveal-melanoma/","tip":"A melanoma inside the eye that is biologically unrelated to skin melanoma: different mutations, no response to standard immunotherapy, and a tendency to spread to the liver years later. Tebentafusp is the first drug ever to extend survival in the metastatic disease."},{"label":"Synovial sarcoma","href":"/cancers/synovial-sarcoma/","tip":"Synovial sarcoma is a young person's sarcoma driven by a single fusion gene, SS18-SSX, that scrambles how genes are switched on. It is treated with surgery, radiotherapy and ifosfamide-based chemotherapy, and in 2024 it became the first solid tumour with an approved engineered T-cell receptor therapy."},{"label":"Melanoma","href":"/cancers/melanoma/","tip":"The skin cancer that proved immunotherapy works: half of advanced patients now live 10 years. Also the first with an approved TIL therapy, an oncolytic virus, and a positive phase 3 personalised vaccine."}],"tags":[{"label":"hla","href":"/tagged/hla/","tip":"Every record tagged hla."}]},"sortKeys":{"year":0}},{"id":"hrr-gene-mutation","name":"Homologous recombination repair gene mutation in prostate cancer","tldr":"A fault in one of the genes a cell uses to mend broken DNA. It decides whether a PARP inhibitor can be prescribed, but the list of genes that counts is different for each of the four approved routes, and the evidence behind them is mostly evidence about BRCA2.","route":"/biomarkers/hrr-gene-mutation/","kind":"biomarker","target":{"id":"brca","name":"BRCA1 / BRCA2 (HRD)","targetClass":"tumor-suppressor","tldr":"DNA repair genes. Inheriting a broken copy raises breast and ovarian cancer risk, but tumours that lose them become uniquely vulnerable to PARP inhibitors and platinum."},"sub":"BRCA1, BRCA2","facets":{"kind":["Biomarker"],"cancers":["Prostate cancer","Metastatic castration-resistant prostate cancer","Metastatic hormone-sensitive prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."},{"label":"Metastatic hormone-sensitive prostate cancer","href":"/cancers/prostate-mhspc/","tip":"Metastatic hormone-sensitive prostate cancer is disease that has spread but still responds to lowering testosterone. Hormone therapy alone is no longer enough: adding an androgen receptor inhibitor, and docetaxel for high-volume disease, lengthens life by years."}],"tags":[{"label":"prostate","href":"/tagged/prostate/","tip":"Every record tagged prostate."}]},"sortKeys":{"year":0}},{"id":"hrd-positive","name":"HRD-positive (genomic instability score)","tldr":"HRD-positive means the tumour's genome carries the scars of failed double-strand break repair (or a BRCA mutation), measured as a genomic instability score. In ovarian cancer it selects niraparib, and olaparib with bevacizumab, as first-line maintenance.","route":"/biomarkers/hrd-positive/","kind":"biomarker","target":{"id":"brca","name":"BRCA1 / BRCA2 (HRD)","targetClass":"tumor-suppressor","tldr":"DNA repair genes. Inheriting a broken copy raises breast and ovarian cancer risk, but tumours that lose them become uniquely vulnerable to PARP inhibitors and platinum."},"sub":"BRCA1, BRCA2","facets":{"kind":["Biomarker"],"cancers":["Ovarian cancer","High-grade serous ovarian cancer","Triple-negative breast cancer","Early triple-negative breast cancer","Pancreatic ductal adenocarcinoma","BRCA or PALB2-mutant pancreatic ductal adenocarcinoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Ovarian cancer","href":"/cancers/ovarian/","tip":"Usually found late. PARP inhibitors transformed maintenance therapy, and ADCs against folate receptor and CDH6 are arriving for platinum-resistant disease."},{"label":"High-grade serous ovarian cancer","href":"/cancers/high-grade-serous-ovarian-cancer/","tip":"High-grade serous cancer is the common, aggressive form of ovarian cancer, now known to start in the fallopian tube. It is treated with surgery and platinum chemotherapy, and maintenance PARP inhibitors have changed its course for the half of patients whose tumours cannot repair DNA properly."},{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."},{"label":"Early triple-negative breast cancer","href":"/cancers/tnbc-early/","tip":"Early triple-negative breast cancer is treated to cure. For tumours over 2 cm or with node involvement, chemotherapy plus the immunotherapy pembrolizumab before and after surgery has raised cure rates; BRCA carriers with cancer left at surgery add a year of olaparib, and others with residual cancer are offered capecitabine. Whether the tumour has vanished by surgery guides what comes next."}],"tags":[{"label":"brca","href":"/tagged/brca/","tip":"Every record tagged brca."},{"label":"genome-wide","href":"/tagged/genome-wide/","tip":"Every record tagged genome-wide."}]},"sortKeys":{"year":0}},{"id":"idh1-r132","name":"IDH1 R132 mutation","tldr":"IDH1 R132 mutations turn a metabolic enzyme into a producer of the oncometabolite 2-HG. They define lower-grade gliomas and occur in acute myeloid leukaemia and bile duct cancer, each with an approved IDH1 inhibitor.","route":"/biomarkers/idh1-r132/","kind":"biomarker","target":{"id":"idh","name":"IDH1 / IDH2","targetClass":"enzyme","tldr":"A metabolic enzyme whose mutant form produces a molecule that scrambles how genes are read; blocking it slows brain tumours and leukaemias."},"sub":"IDH1, IDH2","facets":{"kind":["Biomarker"],"cancers":["Acute myeloid leukaemia","IDH1- and IDH2-mutated acute myeloid leukaemia","Biliary tract cancer","Glioma & glioblastoma","Astrocytoma, IDH-mutant","Oligodendroglioma, IDH-mutant and 1p/19q-codeleted","Myelodysplastic syndromes / neoplasms"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"IDH1- and IDH2-mutated acute myeloid leukaemia","href":"/cancers/aml-idh/","tip":"IDH-mutated acute myeloid leukaemia has a faulty metabolic enzyme that floods cells with a chemical that blocks maturation. Pills that shut the enzyme off, ivosidenib for IDH1 and enasidenib or olutasidenib for IDH2 and IDH1, let the leukaemia cells mature, and ivosidenib with azacitidine tripled survival in older patients."},{"label":"Biliary tract cancer","href":"/cancers/cholangiocarcinoma/","tip":"Cholangiocarcinoma is cancer of the bile ducts or gallbladder. It is rare and often found late, but it turned out to carry more targetable mutations than almost any other gastrointestinal cancer, and immunotherapy now adds to chemotherapy from the first treatment."},{"label":"Glioma & glioblastoma","href":"/cancers/glioblastoma/","tip":"Gliomas are now diagnosed by molecular class, and three classes got their first targeted drugs in 2024-25 (vorasidenib for IDH-mutant glioma, tovorafenib for BRAF-altered paediatric glioma, dordaviprone for H3 K27M). Glioblastoma is the hardest to treat: surgery, radiotherapy with temozolomide and tumour treating fields are its backbone, with CAR-T into the brain and focused ultrasound in trials."}],"tags":[{"label":"idh","href":"/tagged/idh/","tip":"Every record tagged idh."}]},"sortKeys":{"year":0}},{"id":"idh2-mutation","name":"IDH2 mutation (R140 and R172)","tldr":"IDH2 mutations at codons 140 and 172 do the same job as IDH1 R132, producing 2-HG. Enasidenib is approved for relapsed AML with them, and vorasidenib for grade 2 gliomas with either IDH gene mutated.","route":"/biomarkers/idh2-mutation/","kind":"biomarker","target":{"id":"idh","name":"IDH1 / IDH2","targetClass":"enzyme","tldr":"A metabolic enzyme whose mutant form produces a molecule that scrambles how genes are read; blocking it slows brain tumours and leukaemias."},"sub":"IDH1, IDH2","facets":{"kind":["Biomarker"],"cancers":["Acute myeloid leukaemia","IDH1- and IDH2-mutated acute myeloid leukaemia","Astrocytoma, IDH-mutant","Oligodendroglioma, IDH-mutant and 1p/19q-codeleted"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"IDH1- and IDH2-mutated acute myeloid leukaemia","href":"/cancers/aml-idh/","tip":"IDH-mutated acute myeloid leukaemia has a faulty metabolic enzyme that floods cells with a chemical that blocks maturation. Pills that shut the enzyme off, ivosidenib for IDH1 and enasidenib or olutasidenib for IDH2 and IDH1, let the leukaemia cells mature, and ivosidenib with azacitidine tripled survival in older patients."},{"label":"Astrocytoma, IDH-mutant","href":"/cancers/idh-mutant-astrocytoma/","tip":"IDH-mutant astrocytoma is the slow-growing form of adult glioma, defined by a mutation in the IDH1 or IDH2 gene that makes the tumour produce a chemical which rewires its own cells. Surgery first, and then either watchful waiting, the new pill vorasidenib, or radiotherapy with chemotherapy, depending on grade and how much tumour is left."},{"label":"Oligodendroglioma, IDH-mutant and 1p/19q-codeleted","href":"/cancers/oligodendroglioma/","tip":"Oligodendroglioma is the adult brain tumour most responsive to chemotherapy. It is recognised by an IDH mutation together with loss of parts of chromosomes 1 and 19, and after surgery it is treated with radiotherapy plus the PCV drug combination, or, for small grade 2 tumours, with vorasidenib or watchful waiting."}],"tags":[{"label":"idh","href":"/tagged/idh/","tip":"Every record tagged idh."}]},"sortKeys":{"year":0}},{"id":"ig-tcr-clonality","name":"Immunoglobulin and T-cell receptor clonality","tldr":"A test that asks whether a group of lymphocytes all descend from one cell. Cancer is one family; a normal immune response is a crowd. It is used when the appearance under the microscope does not settle the question.","route":"/biomarkers/ig-tcr-clonality/","kind":"biomarker","sub":"Genome-wide readout","facets":{"kind":["Biomarker"],"cancers":["Non-Hodgkin lymphoma","Cutaneous T-cell lymphoma","Sezary syndrome","Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue","Peripheral T-cell lymphomas","Follicular lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."},{"label":"Cutaneous T-cell lymphoma","href":"/cancers/cutaneous-t-cell-lymphoma/","tip":"Cutaneous T-cell lymphoma is a family of nine lymphomas that start in the skin and mostly stay there, of which mycosis fungoides is by far the commonest. Most of them are long-term skin conditions managed over decades rather than cancers that are cured or not cured, and two of the nine are genuinely aggressive."},{"label":"Sezary syndrome","href":"/cancers/sezary-syndrome/","tip":"Sezary syndrome is the leukaemic form of skin lymphoma: the whole skin turns red and scaly, the lymph nodes swell, and malignant T cells circulate in the blood. It is treated to control rather than cure, with photopheresis, the antibody mogamulizumab, and drugs such as bexarotene and interferon, and a stem cell transplant is the only treatment that can cure it in fit patients."},{"label":"Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue","href":"/cancers/malt-lymphoma/","tip":"MALT lymphoma is a slow-growing lymphoma that starts in lymphoid tissue lining an organ, most often the stomach, where it is usually caused by long-standing Helicobacter pylori infection and can be cured with antibiotics alone. Other sites include the eye socket, salivary glands, thyroid, lung and skin; localised disease is treated with low-dose radiotherapy and widespread disease with rituximab."}],"tags":[{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"ki-67-index","name":"Ki-67 index (proliferation by IHC)","tldr":"Ki-67 is the percentage of tumour cells that are dividing. In neuroendocrine tumours it sets the grade; in breast cancer a 20 percent cut-off was briefly a condition of adjuvant abemaciclib, then dropped from the label in 2023.","route":"/biomarkers/ki-67-index/","kind":"biomarker","target":{"id":"mki67","name":"Ki-67 (MKI67)","targetClass":"other","tldr":"Ki-67 is a protein present only in cells that are dividing, so the share of tumour cells that stain for it is a direct read of how fast the cancer is growing."},"sub":"MKI67","facets":{"kind":["Biomarker"],"cancers":["HR-positive / HER2-negative breast cancer","High-risk early HR-positive breast cancer","Neuroendocrine tumours","Pancreatic neuroendocrine tumours","Lung neuroendocrine tumours"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"High-risk early HR-positive breast cancer","href":"/cancers/hr-positive-early-high-risk/","tip":"Most hormone-driven breast cancers are cured with surgery, radiotherapy and five to ten years of endocrine tablets. Women whose tumours are larger, higher grade or have reached the lymph nodes face a higher risk of relapse: two to three years of a CDK4/6 inhibitor added to endocrine therapy cuts recurrence, and genomic tests such as Oncotype DX and MammaPrint decide who also needs chemotherapy."},{"label":"Neuroendocrine tumours","href":"/cancers/neuroendocrine/","tip":"A family of usually slow-growing tumours that start in hormone-producing cells of the gut, pancreas and lungs. They pioneered the idea of using the same molecule to see a tumour on a scan and then to treat it with radiation."},{"label":"Pancreatic neuroendocrine tumours","href":"/cancers/pancreatic-net/","tip":"Pancreatic neuroendocrine tumours arise from the hormone-producing islet cells of the pancreas and behave very differently from ordinary pancreatic cancer, often growing for years. Surgery cures localised tumours; advanced disease is treated in sequence with somatostatin analogues, lutetium-177 dotatate, targeted tablets and oral chemotherapy, and a minority secrete insulin or gastrin."}],"tags":[{"label":"proliferation","href":"/tagged/proliferation/","tip":"Every record tagged proliferation."}]},"sortKeys":{"year":0}},{"id":"kit-d816v","name":"KIT D816V","tldr":"KIT D816V is the mutation behind almost every case of systemic mastocytosis. It makes the disease resistant to imatinib, and it is detected by a highly sensitive blood PCR; avapritinib treats the disease whether or not the mutation is confirmed.","route":"/biomarkers/kit-d816v/","kind":"biomarker","target":{"id":"kit","name":"KIT","targetClass":"kinase","tldr":"KIT mutation is the driver behind most gastrointestinal stromal tumours, and the reason imatinib turned a sarcoma with a median survival of about a year into a chronic disease."},"sub":"KIT","facets":{"kind":["Biomarker"],"cancers":["Systemic mastocytosis","Acute myeloid leukaemia","Gastrointestinal stromal tumour"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Systemic mastocytosis","href":"/cancers/systemic-mastocytosis/","tip":"Systemic mastocytosis is a clonal disease of mast cells, the immune cells that release histamine; almost every case is driven by a single mutation in the KIT gene. Precise KIT-blocking pills now shrink the mast cell burden, ease symptoms and, in the aggressive forms, prolong life. Most patients have the indolent form, where the goal is controlling symptoms and preventing anaphylaxis."},{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"Gastrointestinal stromal tumour","href":"/cancers/gist/","tip":"GIST is a sarcoma of the gut wall driven almost always by a KIT or PDGFRA mutation. It was the proof that a pill can control a solid tumour: imatinib turned a median survival of about a year into one of eight years or more, and the mutation now dictates which drug to use."}],"tags":[{"label":"kit","href":"/tagged/kit/","tip":"Every record tagged kit."}]},"sortKeys":{"year":0}},{"id":"kras-g12c","name":"KRAS G12C","tldr":"KRAS G12C swaps glycine 12 for cysteine and was the first KRAS mutation a drug could grip. Sotorasib and adagrasib are approved for it in lung cancer, and with an EGFR antibody in bowel cancer.","route":"/biomarkers/kras-g12c/","kind":"biomarker","target":{"id":"kras","name":"KRAS","targetClass":"oncogene","tldr":"KRAS is the most commonly mutated cancer gene, called 'undruggable' for 40 years until 2021."},"sub":"KRAS","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Colorectal cancer","Pancreatic ductal adenocarcinoma","KRAS G12C-mutant pancreatic ductal adenocarcinoma","Metastatic pancreatic ductal adenocarcinoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Pancreatic ductal adenocarcinoma","href":"/cancers/pancreatic/","tip":"Almost every pancreatic tumour carries a KRAS mutation, and for the first time drugs against it work: daraxonrasib nearly doubled survival in previously treated disease in 2026. Pancreatic cancer has been the hardest common cancer to treat once advanced; that is what is starting to change."},{"label":"KRAS G12C-mutant pancreatic ductal adenocarcinoma","href":"/cancers/kras-g12c-pdac/","tip":"KRAS G12C pancreatic cancer is the small slice of pancreatic cancer whose KRAS mutation happens to be the one that the first KRAS drugs were built for. Sotorasib and adagrasib, approved for lung cancer, shrink a share of these tumours after chemotherapy and are listed as options, and newer inhibitors such as elironrasib, olomorasib and the pan-RAS drug daraxonrasib are being tested in this group."}],"tags":[{"label":"kras","href":"/tagged/kras/","tip":"Every record tagged kras."}]},"sortKeys":{"year":0}},{"id":"kras-g12d","name":"KRAS G12D (and other non-G12C KRAS mutations)","tldr":"G12D is the commonest KRAS mutation, especially in pancreatic cancer, and has no approved drug yet. In bowel cancer any KRAS or NRAS mutation is a reason not to give EGFR antibodies, which is where the approvals sit.","route":"/biomarkers/kras-g12d/","kind":"biomarker","target":{"id":"kras","name":"KRAS","targetClass":"oncogene","tldr":"KRAS is the most commonly mutated cancer gene, called 'undruggable' for 40 years until 2021."},"sub":"KRAS","facets":{"kind":["Biomarker"],"cancers":["Pancreatic ductal adenocarcinoma","Colorectal cancer","Non-small-cell lung cancer","Metastatic pancreatic ductal adenocarcinoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Pancreatic ductal adenocarcinoma","href":"/cancers/pancreatic/","tip":"Almost every pancreatic tumour carries a KRAS mutation, and for the first time drugs against it work: daraxonrasib nearly doubled survival in previously treated disease in 2026. Pancreatic cancer has been the hardest common cancer to treat once advanced; that is what is starting to change."},{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Metastatic pancreatic ductal adenocarcinoma","href":"/cancers/metastatic-pdac/","tip":"Metastatic pancreatic cancer has spread beyond the pancreas, usually to the liver, and is treated with chemotherapy rather than surgery. Three combination regimens lengthen life, a minority of patients qualify for targeted drugs chosen by tumour or inherited mutations, and in 2026 the pan-RAS inhibitor daraxonrasib became the first drug against the KRAS mutation that drives almost every case."}],"tags":[{"label":"kras","href":"/tagged/kras/","tip":"Every record tagged kras."}]},"sortKeys":{"year":0}},{"id":"met-amplification-readout","name":"MET amplification (gene copy number)","tldr":"MET amplification means extra copies of the MET gene, either as a primary driver in a few lung cancers or as the escape route after EGFR inhibitors. No label yet selects on it; trials define it by FISH ratio or copy number.","route":"/biomarkers/met-amplification-readout/","kind":"biomarker","target":{"id":"met","name":"MET","targetClass":"kinase","tldr":"A receptor that is either mutated in some lung cancers or amplified as an escape route when other lung cancer drugs fail."},"sub":"MET","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Gastric & gastro-oesophageal junction cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Gastric & gastro-oesophageal junction cancer","href":"/cancers/gastric/","tip":"A cancer with three new targets in five years: Claudin 18.2, FGFR2b, and HER2 with new ADCs, plus immunotherapy in first line."}],"tags":[{"label":"met","href":"/tagged/met/","tip":"Every record tagged met."},{"label":"no-approval","href":"/tagged/no-approval/","tip":"Every record tagged no-approval."}]},"sortKeys":{"year":0}},{"id":"met-ex14","name":"MET exon 14 skipping mutation","tldr":"MET exon 14 skipping is a splice-site change that lets the MET receptor escape degradation and keep signalling. It is found in 3 to 4 percent of lung cancers and is treated with capmatinib or tepotinib.","route":"/biomarkers/met-ex14/","kind":"biomarker","target":{"id":"met","name":"MET","targetClass":"kinase","tldr":"A receptor that is either mutated in some lung cancers or amplified as an escape route when other lung cancer drugs fail."},"sub":"MET","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"met","href":"/tagged/met/","tip":"Every record tagged met."}]},"sortKeys":{"year":0}},{"id":"mgmt-promoter-methylation","name":"MGMT promoter methylation","tldr":"Methylation of the MGMT promoter switches off the repair enzyme that undoes temozolomide's damage. Methylated glioblastomas live longer on temozolomide; unmethylated ones gain little, and trials now use the result to spare or intensify chemotherapy.","route":"/biomarkers/mgmt-promoter-methylation/","kind":"biomarker","target":{"id":"mgmt-protein","name":"MGMT (O6-methylguanine-DNA methyltransferase)","targetClass":"enzyme","tldr":"MGMT is a DNA repair enzyme that removes the damage temozolomide causes; when the gene is switched off by methylation the tumour cannot repair itself and the drug works better."},"sub":"MGMT","facets":{"kind":["Biomarker"],"cancers":["Glioma & glioblastoma","Astrocytoma, IDH-mutant"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Glioma & glioblastoma","href":"/cancers/glioblastoma/","tip":"Gliomas are now diagnosed by molecular class, and three classes got their first targeted drugs in 2024-25 (vorasidenib for IDH-mutant glioma, tovorafenib for BRAF-altered paediatric glioma, dordaviprone for H3 K27M). Glioblastoma is the hardest to treat: surgery, radiotherapy with temozolomide and tumour treating fields are its backbone, with CAR-T into the brain and focused ultrasound in trials."},{"label":"Astrocytoma, IDH-mutant","href":"/cancers/idh-mutant-astrocytoma/","tip":"IDH-mutant astrocytoma is the slow-growing form of adult glioma, defined by a mutation in the IDH1 or IDH2 gene that makes the tumour produce a chemical which rewires its own cells. Surgery first, and then either watchful waiting, the new pill vorasidenib, or radiotherapy with chemotherapy, depending on grade and how much tumour is left."}],"tags":[{"label":"methylation","href":"/tagged/methylation/","tip":"Every record tagged methylation."},{"label":"no-approval","href":"/tagged/no-approval/","tip":"Every record tagged no-approval."}]},"sortKeys":{"year":0}},{"id":"msi-high","name":"MSI-high (microsatellite instability by PCR or sequencing)","tldr":"MSI-high means the tumour's DNA has unstable repeat sequences, the footprint of failed mismatch repair. It is measured by PCR or sequencing, gives the same answer as dMMR in most tumours, and unlocks the same immunotherapies.","route":"/biomarkers/msi-high/","kind":"biomarker","target":{"id":"mmr","name":"Mismatch repair proteins (MLH1, MSH2, MSH6, PMS2)","targetClass":"enzyme","tldr":"The four mismatch repair proteins proofread newly copied DNA; when a tumour loses one of them its DNA fills with small errors, and that state (dMMR or MSI-high) is what lets immunotherapy work across many cancers."},"sub":"MLH1, MSH2, MSH6, PMS2","facets":{"kind":["Biomarker"],"cancers":["Colorectal cancer","Endometrial cancer","Mismatch-repair-deficient endometrial cancer","Microsatellite-unstable (MSI-high) gastric cancer","Metastatic cancer","Triple-negative breast cancer","Pancreatic ductal adenocarcinoma","Mismatch repair deficient (MSI-high) pancreatic ductal adenocarcinoma","Gallbladder cancer","Biliary tract cancer","Prostate cancer","Metastatic castration-resistant prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Endometrial cancer","href":"/cancers/endometrial/","tip":"The gynaecological cancer where immunotherapy has had the biggest impact, guided by molecular classification."},{"label":"Mismatch-repair-deficient endometrial cancer","href":"/cancers/endometrial-mmr-deficient/","tip":"Mismatch-repair-deficient endometrial cancer has lost the machinery that corrects copying errors in DNA, so it accumulates thousands of mutations that make it visible to the immune system. Adding dostarlimab or pembrolizumab to chemotherapy in advanced disease cut the risk of progression by about seventy percent, and many patients remain in remission years later."},{"label":"Microsatellite-unstable (MSI-high) gastric cancer","href":"/cancers/gastric-msi-high/","tip":"Microsatellite-unstable gastric cancer has lost its DNA mismatch repair machinery, carries thousands of mutations and is unusually visible to the immune system. It responds strongly to checkpoint antibodies, may gain little from chemotherapy, and in early-stage disease immunotherapy before surgery is making many tumours disappear entirely."}],"tags":[{"label":"mmr","href":"/tagged/mmr/","tip":"Every record tagged mmr."}]},"sortKeys":{"year":0}},{"id":"mycn-amp","name":"MYCN amplification","tldr":"MYCN amplification, more than four times the normal copy number of the gene on FISH, marks the most aggressive fifth of neuroblastomas and puts a child in the high-risk group whatever their age or stage. No drug targets it; it decides how much treatment is given.","route":"/biomarkers/mycn-amp/","kind":"biomarker","target":{"id":"mycn","name":"MYCN (N-myc)","targetClass":"transcription","tldr":"MYCN is a growth-driving gene that some neuroblastomas copy many times over; that amplification is one of the strongest signs the tumour is aggressive and sets the intensity of treatment."},"sub":"MYCN","facets":{"kind":["Biomarker"],"cancers":["Neuroblastoma","High-risk neuroblastoma","Intermediate-risk neuroblastoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Neuroblastoma","href":"/cancers/neuroblastoma/","tip":"Neuroblastoma is a childhood nerve-cell cancer where anti-GD2 antibodies and, recently, GD2 CAR-T have improved survival in high-risk disease."},{"label":"High-risk neuroblastoma","href":"/cancers/neuroblastoma-high-risk/","tip":"High-risk neuroblastoma has spread widely in a child over 18 months old or carries extra copies of the MYCN gene. Treatment lasts about 18 months and uses every tool: chemotherapy, surgery, high-dose chemotherapy with stem cell rescue, radiotherapy, and the anti-GD2 antibody dinutuximab, which raised survival in ANBL0032; eflornithine, given afterwards, was approved in 2023 to lower relapse."},{"label":"Intermediate-risk neuroblastoma","href":"/cancers/neuroblastoma-intermediate-risk/","tip":"Intermediate-risk neuroblastoma sits between the tumours that go away on their own and the high-risk disease that needs everything. A few cycles of moderate chemotherapy followed by surgery cure most children, and trials have spent twenty years showing how few cycles are enough."}],"tags":[{"label":"paediatric","href":"/tagged/paediatric/","tip":"Every record tagged paediatric."},{"label":"no-approval","href":"/tagged/no-approval/","tip":"Every record tagged no-approval."}]},"sortKeys":{"year":0}},{"id":"nectin-4-expression","name":"Nectin-4 expression","tldr":"Nectin-4 is expressed by almost every urothelial cancer, so enfortumab vedotin is given without a test. Nectin-4 amplification is being studied as a marker of especially strong response.","route":"/biomarkers/nectin-4-expression/","kind":"biomarker","target":{"id":"nectin4","name":"Nectin-4","targetClass":"surface-antigen","tldr":"Nectin-4 is an adhesion protein plentiful on bladder cancer cells, used as the docking site for the ADC enfortumab vedotin."},"sub":"NECTIN4","facets":{"kind":["Biomarker"],"cancers":["Bladder & urothelial cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Bladder & urothelial cancer","href":"/cancers/urothelial/","tip":"Bladder cancer went from 40 years of cisplatin to an ADC-immunotherapy combination that nearly doubled survival, and in 2026 the first blood-test-guided drug approval."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"npm1-mutation","name":"NPM1 mutation","tldr":"NPM1 mutations, found in about a third of adult acute myeloid leukaemias, misplace the nucleophosmin protein into the cytoplasm. They mean a better outlook without FLT3-ITD, a sensitive MRD marker, and since 2025 a targeted menin inhibitor.","route":"/biomarkers/npm1-mutation/","kind":"biomarker","target":{"id":"npm1","name":"NPM1 mutation","targetClass":"other","tldr":"NPM1 is the most common mutation in adult leukaemia. It moves a nuclear protein into the cytoplasm and, it turns out, makes the leukaemia dependent on menin."},"sub":"NPM1","facets":{"kind":["Biomarker"],"cancers":["Acute myeloid leukaemia","NPM1-mutated and KMT2A-rearranged acute myeloid leukaemia"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"NPM1-mutated and KMT2A-rearranged acute myeloid leukaemia","href":"/cancers/aml-npm1-kmt2a/","tip":"NPM1-mutated and KMT2A-rearranged leukaemias depend on a protein called menin to keep leukaemia genes switched on. Menin inhibitors, revumenib and ziftomenib, are the first drugs to exploit this, and they produce remissions in patients whose leukaemia had come back after everything else."}],"tags":[{"label":"aml","href":"/tagged/aml/","tip":"Every record tagged aml."}]},"sortKeys":{"year":0}},{"id":"nrg1-fusion","name":"NRG1 gene fusion","tldr":"A rare fusion that joins the neuregulin 1 gene to a partner, leaving the HER3 ligand stuck on the cell surface where it switches HER3 on continuously. It is found in a small percentage of lung adenocarcinomas, particularly invasive mucinous adenocarcinoma in people who have never smoked, and in pancreatic and biliary cancers, and zenocutuzumab is approved for it.","route":"/biomarkers/nrg1-fusion/","kind":"biomarker","target":{"id":"her3","name":"HER3","targetClass":"surface-antigen","tldr":"HER3 is a cousin of HER2 that cancers use as an escape route when HER2 or EGFR are blocked."},"sub":"ERBB3","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Pancreatic ductal adenocarcinoma","Biliary tract cancer","Invasive mucinous adenocarcinoma of the lung","Lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Pancreatic ductal adenocarcinoma","href":"/cancers/pancreatic/","tip":"Almost every pancreatic tumour carries a KRAS mutation, and for the first time drugs against it work: daraxonrasib nearly doubled survival in previously treated disease in 2026. Pancreatic cancer has been the hardest common cancer to treat once advanced; that is what is starting to change."},{"label":"Biliary tract cancer","href":"/cancers/cholangiocarcinoma/","tip":"Cholangiocarcinoma is cancer of the bile ducts or gallbladder. It is rare and often found late, but it turned out to carry more targetable mutations than almost any other gastrointestinal cancer, and immunotherapy now adds to chemotherapy from the first treatment."},{"label":"Invasive mucinous adenocarcinoma of the lung","href":"/cancers/invasive-mucinous-adenocarcinoma-lung/","tip":"Invasive mucinous adenocarcinoma is a type of lung cancer whose cells look like stomach or bowel lining and fill the air spaces with mucus, often appearing as pneumonia-like shadows on a scan. Most cases carry a KRAS mutation, and many of the rest carry a gene fusion, including NRG1, that new drugs can target."}],"tags":[{"label":"fusion","href":"/tagged/fusion/","tip":"Every record tagged fusion."}]},"sortKeys":{"year":0}},{"id":"ntrk-fusion","name":"NTRK1/2/3 gene fusion","tldr":"An NTRK fusion joins one of three TRK kinase genes to a partner and drives cancers from infant fibrosarcoma to salivary and thyroid tumours, rare in common cancers but near-universal in a few rare ones. Larotrectinib, entrectinib and repotrectinib are approved for it regardless of tumour type.","route":"/biomarkers/ntrk-fusion/","kind":"biomarker","target":{"id":"ntrk","name":"NTRK","targetClass":"kinase","tldr":"Rare gene fusions found across dozens of cancer types; the first target where a drug was approved for any tumour carrying it."},"sub":"NTRK1/2/3","facets":{"kind":["Biomarker"],"cancers":["Metastatic cancer","Sarcomas","Thyroid cancer","Salivary gland cancers","Colorectal cancer","Non-small-cell lung cancer","Pancreatic ductal adenocarcinoma","KRAS wild-type pancreatic ductal adenocarcinoma","Gallbladder cancer","Biliary tract cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Metastatic cancer","href":"/cancers/metastatic-cancer/","tip":"Metastatic cancer means the original cancer has spread to other parts of the body, most often the bones, liver, lungs or brain. It keeps the name of where it started, is treated with therapies that reach the whole body, and can increasingly be controlled for years; with limited spread it is sometimes treated with the aim of cure."},{"label":"Sarcomas","href":"/cancers/sarcoma/","tip":"Sarcomas are dozens of rare cancers of bone and connective tissue. GIST was the first solid tumour cured-in-practice by a targeted pill; synovial sarcoma got the first TCR-T therapy."},{"label":"Thyroid cancer","href":"/cancers/thyroid/","tip":"Thyroid cancer is usually curable with surgery and radioactive iodine, the original theranostic. Rare aggressive forms respond to RET and BRAF inhibitors."},{"label":"Salivary gland cancers","href":"/cancers/salivary-gland/","tip":"Salivary gland cancers are a family of over 20 rare cancers, each with its own behaviour and often its own gene fusion. Surgery and radiation treat most; drug therapy is now chosen by the specific subtype, from anti-HER2 or anti-androgen drugs to NTRK inhibitors."}],"tags":[{"label":"fusion","href":"/tagged/fusion/","tip":"Every record tagged fusion."}]},"sortKeys":{"year":0}},{"id":"pdl1","name":"PD-L1","tldr":"PD-L1 is the tumour's side of the PD-1 brake, and also the biomarker that decides who gets immunotherapy.","route":"/targets/pdl1/","kind":"target","target":{"id":"pdl1","name":"PD-L1","targetClass":"checkpoint","tldr":"PD-L1 is the tumour's side of the PD-1 brake, and also the biomarker that decides who gets immunotherapy."},"sub":"CD274","facets":{"kind":["Target"],"cancers":["Triple-negative breast cancer","Non-small-cell lung cancer","Bladder & urothelial cancer","Small-cell lung cancer","Gallbladder cancer","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Target","tip":"The molecules drugs and tracers aim at."},"cancers":[{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."},{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Bladder & urothelial cancer","href":"/cancers/urothelial/","tip":"Bladder cancer went from 40 years of cisplatin to an ADC-immunotherapy combination that nearly doubled survival, and in 2026 the first blood-test-guided drug approval."},{"label":"Small-cell lung cancer","href":"/cancers/sclc/","tip":"A fast-growing lung cancer. About a third of cases are confined to one side of the chest and are treated to cure with chemotherapy and radiotherapy together; the rest respond to chemotherapy and relapse quickly. After 30 years without progress, durvalumab consolidation, the T-cell engager tarlatamab and antibody-drug conjugates have each lengthened survival since 2024."}],"tags":[{"label":"checkpoint","href":"/tagged/checkpoint/","tip":"Every record tagged checkpoint."}]},"sortKeys":{"year":0}},{"id":"pd-l1-cps","name":"PD-L1 CPS (combined positive score)","tldr":"CPS counts every PD-L1-stained cell in the tumour, immune cells included, and divides by the number of tumour cells. Pembrolizumab labels use CPS 1 or CPS 10 as the gate in head and neck, stomach, oesophageal, cervical, ovarian and triple-negative breast cancer.","route":"/biomarkers/pd-l1-cps/","kind":"biomarker","target":{"id":"pdl1","name":"PD-L1","targetClass":"checkpoint","tldr":"PD-L1 is the tumour's side of the PD-1 brake, and also the biomarker that decides who gets immunotherapy."},"sub":"CD274","facets":{"kind":["Biomarker"],"cancers":["Head and neck squamous cell carcinoma","Gastric & gastro-oesophageal junction cancer","HER2-positive gastric cancer","PD-L1-high gastric cancer","Oesophageal cancer","Oesophageal squamous cell carcinoma","Cervical cancer","Triple-negative breast cancer","Metastatic triple-negative breast cancer","Ovarian cancer","Platinum-resistant ovarian cancer","Gallbladder cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Head and neck squamous cell carcinoma","href":"/cancers/head-and-neck/","tip":"Cancers of the mouth and throat, increasingly caused by HPV. Immunotherapy is first line for advanced disease and now used before surgery."},{"label":"Gastric & gastro-oesophageal junction cancer","href":"/cancers/gastric/","tip":"A cancer with three new targets in five years: Claudin 18.2, FGFR2b, and HER2 with new ADCs, plus immunotherapy in first line."},{"label":"HER2-positive gastric cancer","href":"/cancers/gastric-her2-positive/","tip":"HER2-positive gastric cancer overexpresses the HER2 growth receptor and is treated with trastuzumab added to chemotherapy, now usually with pembrolizumab as well. After progression the antibody-drug conjugate trastuzumab deruxtecan gives responses that plain chemotherapy cannot."},{"label":"PD-L1-high gastric cancer","href":"/cancers/gastric-pdl1-high/","tip":"PD-L1-high gastric cancer expresses the immune checkpoint protein PD-L1 on tumour and immune cells, and this is the group in which nivolumab or pembrolizumab added to chemotherapy clearly extends life. The benefit shrinks as the score falls, so regulators now restrict the antibodies to tumours with at least some PD-L1 expression."}],"tags":[{"label":"pd-l1","href":"/tagged/pd-l1/","tip":"Every record tagged pd-l1."}]},"sortKeys":{"year":0}},{"id":"pd-l1-ic-score","name":"PD-L1 IC score (immune-cell score, SP142)","tldr":"The IC score measures how much of the tumour area is covered by PD-L1-stained immune cells rather than tumour cells. It belongs to the SP142 assay used with atezolizumab and is read differently from every other PD-L1 score.","route":"/biomarkers/pd-l1-ic-score/","kind":"biomarker","target":{"id":"pdl1","name":"PD-L1","targetClass":"checkpoint","tldr":"PD-L1 is the tumour's side of the PD-1 brake, and also the biomarker that decides who gets immunotherapy."},"sub":"CD274","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Bladder & urothelial cancer","Metastatic triple-negative breast cancer","Triple-negative breast cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Bladder & urothelial cancer","href":"/cancers/urothelial/","tip":"Bladder cancer went from 40 years of cisplatin to an ADC-immunotherapy combination that nearly doubled survival, and in 2026 the first blood-test-guided drug approval."},{"label":"Metastatic triple-negative breast cancer","href":"/cancers/tnbc-metastatic/","tip":"The treatment of triple-negative breast cancer that has spread has been transformed since 2020, though it is not yet curable. By PD-L1 score, first treatment is pembrolizumab with chemotherapy or with sacituzumab govitecan, or datopotamab deruxtecan or sacituzumab govitecan alone; BRCA carriers can take a PARP inhibitor tablet; and trastuzumab deruxtecan reaches the third of tumours with low HER2."},{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."}],"tags":[{"label":"pd-l1","href":"/tagged/pd-l1/","tip":"Every record tagged pd-l1."}]},"sortKeys":{"year":0}},{"id":"pd-l1-tc-score","name":"PD-L1 TC score (tumour-cell score, SP263 and 28-8)","tldr":"The TC score is the percentage of tumour cells staining for PD-L1 on the SP263 or 28-8 assays. Atezolizumab uses 1 percent after lung surgery and 50 percent for first-line treatment alone; nivolumab with ipilimumab uses 1 percent in first-line lung cancer.","route":"/biomarkers/pd-l1-tc-score/","kind":"biomarker","target":{"id":"pdl1","name":"PD-L1","targetClass":"checkpoint","tldr":"PD-L1 is the tumour's side of the PD-1 brake, and also the biomarker that decides who gets immunotherapy."},"sub":"CD274","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"pd-l1","href":"/tagged/pd-l1/","tip":"Every record tagged pd-l1."}]},"sortKeys":{"year":0}},{"id":"pd-l1-tps","name":"PD-L1 TPS (tumour proportion score)","tldr":"TPS is the share of tumour cells whose membrane stains for PD-L1, ignoring immune cells. In lung cancer it decides whether pembrolizumab or cemiplimab can be given alone: 1 percent opens the door, 50 percent is where single-agent treatment is strongest.","route":"/biomarkers/pd-l1-tps/","kind":"biomarker","target":{"id":"pdl1","name":"PD-L1","targetClass":"checkpoint","tldr":"PD-L1 is the tumour's side of the PD-1 brake, and also the biomarker that decides who gets immunotherapy."},"sub":"CD274","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Lung cancer","Gallbladder cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Lung cancer","href":"/cancers/lung-cancer/","tip":"Lung cancer splits into non-small-cell disease, about 85 percent of it, and small-cell disease, which was 6.6 percent of English cases in 2024 and 9.1 percent of Welsh ones (National Lung Cancer Audit, State of the Nation 2026); the two behave and are treated very differently. Screening, staging and the things both types share are common ground; the rest belongs to each subtype."},{"label":"Gallbladder cancer","href":"/cancers/gallbladder/","tip":"Gallbladder cancer starts in the small bile-storing sac under the liver and is one of the biliary tract cancers. Most cases are found late, or by chance when a gallbladder is removed for gallstones. It is rare in the UK, with about 1,300 cases a year, and much commoner in Chile, Bolivia and northern India. Found early, an operation can cure it."}],"tags":[{"label":"pd-l1","href":"/tagged/pd-l1/","tip":"Every record tagged pd-l1."}]},"sortKeys":{"year":0}},{"id":"pdgfra-exon-18-d842v","name":"PDGFRA exon 18 mutation (D842V)","tldr":"PDGFRA D842V drives about 5 percent of gastrointestinal stromal tumours and is resistant to imatinib. Avapritinib is the approved drug for GISTs with PDGFRA exon 18 mutations including D842V.","route":"/biomarkers/pdgfra-exon-18-d842v/","kind":"biomarker","target":{"id":"pdgfra","name":"PDGFRA","targetClass":"kinase","tldr":"PDGFRA is a growth-factor receptor mutated in about 10% of GISTs, including the D842V mutation that resists imatinib but responds to avapritinib."},"sub":"PDGFRA","facets":{"kind":["Biomarker"],"cancers":["Gastrointestinal stromal tumour","PDGFRA D842V-mutant GIST"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Gastrointestinal stromal tumour","href":"/cancers/gist/","tip":"GIST is a sarcoma of the gut wall driven almost always by a KIT or PDGFRA mutation. It was the proof that a pill can control a solid tumour: imatinib turned a median survival of about a year into one of eight years or more, and the mutation now dictates which drug to use."},{"label":"PDGFRA D842V-mutant GIST","href":"/cancers/gist-pdgfra-d842v/","tip":"PDGFRA D842V GIST is driven by a mutation in the PDGFRA receptor rather than KIT, and it does not respond to imatinib at all. Avapritinib, designed to fit the mutant activation loop, shrinks nearly nine in ten of these tumours and is the standard treatment for advanced disease; localised tumours are cured by surgery alone."}],"tags":[{"label":"gist","href":"/tagged/gist/","tip":"Every record tagged gist."}]},"sortKeys":{"year":0}},{"id":"pik3ca-hotspot-mutation","name":"PIK3CA mutation","tldr":"PIK3CA mutations in the helical and kinase domains are found in about 40 percent of hormone-receptor-positive breast cancers. Alpelisib, inavolisib and capivasertib are approved for tumours that carry them.","route":"/biomarkers/pik3ca-hotspot-mutation/","kind":"biomarker","target":{"id":"pik3ca","name":"PIK3CA / PI3K-alpha","targetClass":"kinase","tldr":"PIK3CA is the most commonly mutated gene in hormone-driven breast cancer. Drugs against it work, but hitting it cleanly without raising blood sugar took years."},"sub":"PIK3CA","facets":{"kind":["Biomarker"],"cancers":["HR-positive / HER2-negative breast cancer","HR-positive metastatic breast cancer after CDK4/6 inhibitors","Endometrial cancer","Triple-negative breast cancer","Colorectal cancer","Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"HR-positive metastatic breast cancer after CDK4/6 inhibitors","href":"/cancers/hr-positive-metastatic-post-cdk46/","tip":"When hormone-positive breast cancer grows through a CDK4/6 inhibitor, a blood test picks the next drug. Tumours with an acquired ESR1 mutation respond to the oral degraders elacestrant, camizestrant and imlunestrant; tumours with PIK3CA, AKT1 or PTEN changes to capivasertib, inavolisib or alpelisib; and once endocrine options run out, antibody-drug conjugates come before chemotherapy."},{"label":"Endometrial cancer","href":"/cancers/endometrial/","tip":"The gynaecological cancer where immunotherapy has had the biggest impact, guided by molecular classification."},{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."}],"tags":[{"label":"pi3k","href":"/tagged/pi3k/","tip":"Every record tagged pi3k."}]},"sortKeys":{"year":0}},{"id":"plasma-ebv-dna","name":"Plasma EBV DNA","tldr":"Fragments of Epstein-Barr virus DNA in the blood that measure nasopharyngeal carcinoma: used to screen healthy people in endemic regions, to stage, to decide who needs extra treatment after radiotherapy, and to detect relapse.","route":"/terms/plasma-ebv-dna/","kind":"term","term":{"category":"Biomarkers"},"facets":{"kind":["Term"],"cancers":["Hodgkin lymphoma","Peripheral T-cell lymphomas","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Term","tip":"Glossary with plain-English TL;DRs and Wikipedia links."},"cancers":[{"label":"Hodgkin lymphoma","href":"/cancers/hodgkin-lymphoma/","tip":"Hodgkin lymphoma is one of the most curable cancers, where the goal is now to cure with less toxicity, using brentuximab and, from 2026, first-line nivolumab."},{"label":"Peripheral T-cell lymphomas","href":"/cancers/peripheral-t-cell-lymphoma/","tip":"Peripheral T-cell lymphomas are lymphomas of T cells rather than B cells. They are rarer, more varied and, apart from a few subtypes, harder to treat than B-cell lymphomas; several new drugs help only defined subtypes."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."}],"tags":[]},"sortKeys":{"year":0}},{"id":"pr-status","name":"PR status (progesterone receptor by IHC)","tldr":"PR status is read the same way as ER: 1 percent or more of nuclei staining is positive. It is measured alongside ER, adds to prognosis, and a tumour positive for either receptor counts as hormone-receptor-positive.","route":"/biomarkers/pr-status/","kind":"biomarker","target":{"id":"pgr","name":"Progesterone receptor (PGR)","targetClass":"nuclear-receptor","tldr":"The progesterone receptor is the hormone receptor that, alongside the oestrogen receptor, marks breast cancers likely to respond to hormone therapy, and it is the target of the progestins megestrol and medroxyprogesterone used in endometrial and breast cancer."},"sub":"PGR","facets":{"kind":["Biomarker"],"cancers":["HR-positive / HER2-negative breast cancer","Breast cancer","Endometrial cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Breast cancer","href":"/cancers/breast-cancer/","tip":"Breast cancer is not one disease, and the result that decides which page you need is the receptor result: whether the cancer carries oestrogen and progesterone receptors, and whether it carries too much HER2. Those two answers give four boxes, not three, with a page for each. Grade and stage do not change which page you read; they change what happens on it."},{"label":"Endometrial cancer","href":"/cancers/endometrial/","tip":"The gynaecological cancer where immunotherapy has had the biggest impact, guided by molecular classification."}],"tags":[{"label":"hormone-receptor","href":"/tagged/hormone-receptor/","tip":"Every record tagged hormone-receptor."}]},"sortKeys":{"year":0}},{"id":"psma-pet-expression","name":"PSMA expression by PET (PSMA-positive)","tldr":"PSMA-positive means prostate cancer deposits light up on a PSMA PET scan more than the liver does. It is the entry ticket for lutetium-177 PSMA therapy and the basis of the imaging that now stages most advanced prostate cancer.","route":"/biomarkers/psma-pet-expression/","kind":"biomarker","target":{"id":"psma","name":"PSMA","targetClass":"surface-antigen","tldr":"A protein on prostate cancer cells that lets doctors both see the cancer on a PET scan and hit it with a radioactive drug."},"sub":"FOLH1","facets":{"kind":["Biomarker"],"cancers":["Prostate cancer","Metastatic castration-resistant prostate cancer","Metastatic hormone-sensitive prostate cancer","Biochemical recurrence of prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."},{"label":"Metastatic hormone-sensitive prostate cancer","href":"/cancers/prostate-mhspc/","tip":"Metastatic hormone-sensitive prostate cancer is disease that has spread but still responds to lowering testosterone. Hormone therapy alone is no longer enough: adding an androgen receptor inhibitor, and docetaxel for high-volume disease, lengthens life by years."},{"label":"Biochemical recurrence of prostate cancer","href":"/cancers/prostate-bcr/","tip":"Biochemical recurrence of prostate cancer is a rising PSA after surgery or radiotherapy with nothing yet visible on scans. Salvage radiotherapy can still cure it after surgery, and for a fast-doubling PSA the EMBARK trial showed that enzalutamide with or without hormone therapy delays spread."}],"tags":[{"label":"pet","href":"/tagged/pet/","tip":"Every record tagged pet."}]},"sortKeys":{"year":0}},{"id":"pten-alteration","name":"PTEN alteration (sequencing) and PTEN loss (IHC)","tldr":"PTEN can be lost by mutation or deletion (read by sequencing) or as absent protein on a stain. Both readouts select capivasertib: alterations in breast cancer, and protein deficiency in metastatic hormone-sensitive prostate cancer.","route":"/biomarkers/pten-alteration/","kind":"biomarker","target":{"id":"pten","name":"PTEN","targetClass":"tumor-suppressor","tldr":"PTEN is the brake on the PI3K growth pathway; when a tumour loses it the pathway runs unchecked, which is why PTEN loss now selects patients for the AKT inhibitor capivasertib."},"sub":"PTEN","facets":{"kind":["Biomarker"],"cancers":["HR-positive / HER2-negative breast cancer","Metastatic hormone-sensitive prostate cancer","Prostate cancer","Endometrial cancer","Glioma & glioblastoma","Triple-negative breast cancer","Metastatic triple-negative breast cancer","Metastatic castration-resistant prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Metastatic hormone-sensitive prostate cancer","href":"/cancers/prostate-mhspc/","tip":"Metastatic hormone-sensitive prostate cancer is disease that has spread but still responds to lowering testosterone. Hormone therapy alone is no longer enough: adding an androgen receptor inhibitor, and docetaxel for high-volume disease, lengthens life by years."},{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Endometrial cancer","href":"/cancers/endometrial/","tip":"The gynaecological cancer where immunotherapy has had the biggest impact, guided by molecular classification."}],"tags":[{"label":"pi3k","href":"/tagged/pi3k/","tip":"Every record tagged pi3k."}]},"sortKeys":{"year":0}},{"id":"ras-wild-type","name":"RAS wild-type (extended KRAS and NRAS testing)","tldr":"RAS wild-type is the absence of a mutation, and it is the result that decides whether the EGFR antibodies cetuximab and panitumumab can be given in bowel cancer. Extended testing means KRAS and NRAS exons 2, 3 and 4, not just codons 12 and 13.","route":"/biomarkers/ras-wild-type/","kind":"biomarker","target":{"id":"kras","name":"KRAS","targetClass":"oncogene","tldr":"KRAS is the most commonly mutated cancer gene, called 'undruggable' for 40 years until 2021."},"sub":"KRAS","facets":{"kind":["Biomarker"],"cancers":["Colorectal cancer","Rectal cancer","Colon cancer","HER2-amplified colorectal cancer","BRAF V600E-mutant colorectal cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Colorectal cancer","href":"/cancers/colorectal/","tip":"The cancer where screening works best and where immunotherapy can make some tumours disappear entirely; chemotherapy still carries most metastatic disease, now with antibodies and targeted combinations chosen by RAS, BRAF, mismatch repair and which side of the bowel the tumour started on."},{"label":"Rectal cancer","href":"/cancers/rectal-cancer/","tip":"Rectal cancer is bowel cancer in the last part of the large intestine, where surgery can mean a permanent stoma. Treatment now usually gives all the chemotherapy and radiotherapy first, and about half of people whose tumour disappears completely can keep their rectum and avoid surgery altogether."},{"label":"Colon cancer","href":"/cancers/colon-cancer/","tip":"Colon cancer is bowel cancer arising in the large bowel above the rectum. It shares its biology with colorectal cancer but is treated differently from rectal cancer: surgery comes first without radiotherapy, chemotherapy afterwards is decided by stage and increasingly by a blood test for leftover tumour DNA, and the side the tumour started on changes which drugs work once it has spread."},{"label":"HER2-amplified colorectal cancer","href":"/cancers/her2-amplified-colorectal/","tip":"A few bowel cancers make too much of the HER2 protein, the same target as in HER2-positive breast cancer. Two HER2 drugs together, tucatinib and trastuzumab, shrink about four in ten of these tumours after chemotherapy has failed, and the antibody-drug conjugate trastuzumab deruxtecan works even when other HER2 drugs have stopped."}],"tags":[{"label":"kras","href":"/tagged/kras/","tip":"Every record tagged kras."},{"label":"negative-selector","href":"/tagged/negative-selector/","tip":"Every record tagged negative-selector."}]},"sortKeys":{"year":0}},{"id":"ret-fusion","name":"RET fusion and RET mutation","tldr":"RET fusions drive 1 to 2 percent of lung cancers and some thyroid cancers; RET point mutations drive medullary thyroid cancer. Selpercatinib is approved for RET fusions in any solid tumour and for RET-mutant medullary thyroid cancer; pralsetinib for RET fusion lung cancer.","route":"/biomarkers/ret-fusion/","kind":"biomarker","target":{"id":"ret","name":"RET","targetClass":"kinase","tldr":"RET is a kinase altered in thyroid cancer and a small slice of lung cancer, treatable with one selective pill regardless of where the tumour is."},"sub":"RET","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer","Thyroid cancer","Medullary thyroid cancer","Papillary thyroid cancer","Metastatic cancer","Colorectal cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Thyroid cancer","href":"/cancers/thyroid/","tip":"Thyroid cancer is usually curable with surgery and radioactive iodine, the original theranostic. Rare aggressive forms respond to RET and BRAF inhibitors."},{"label":"Medullary thyroid cancer","href":"/cancers/medullary-thyroid-cancer/","tip":"Medullary thyroid cancer comes from the calcitonin-making C cells, not the thyroid hormone cells, so radioactive iodine does not work. Surgery is the only cure, a quarter of cases run in families through the RET gene, and the RET-selective drug selpercatinib has transformed treatment of advanced disease."},{"label":"Papillary thyroid cancer","href":"/cancers/papillary-thyroid-cancer/","tip":"Papillary thyroid cancer is the commonest and most curable thyroid cancer. Most people are treated with surgery, some with radioactive iodine afterwards, and many small tumours can simply be watched. Only the rare tumours that stop taking up iodine need targeted drugs."}],"tags":[{"label":"fusion","href":"/tagged/fusion/","tip":"Every record tagged fusion."}]},"sortKeys":{"year":0}},{"id":"rhoa-g17v","name":"RHOA G17V","tldr":"A single change in a small signalling protein, found in about two thirds of one kind of T-cell lymphoma. It is useful because it is specific to the tumour cells, while the other mutations in the same disease are also present in normal blood cells.","route":"/biomarkers/rhoa-g17v/","kind":"biomarker","target":{"id":"rhoa","name":"RHOA","targetClass":"enzyme","tldr":"RHOA (Transforming protein RhoA) is an enzyme. The public catalogues list it as an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Gastric & gastro-oesophageal junction cancer, Bladder & urothelial cancer and 5 more."},"sub":"RHOA","facets":{"kind":["Biomarker"],"cancers":["Nodal T-follicular helper cell lymphoma, angioimmunoblastic type","Peripheral T-cell lymphomas","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Nodal T-follicular helper cell lymphoma, angioimmunoblastic type","href":"/cancers/angioimmunoblastic-t-cell-lymphoma/","tip":"Angioimmunoblastic T-cell lymphoma, now called nodal T-follicular helper cell lymphoma of angioimmunoblastic type, is one of the commonest T-cell lymphomas and mostly affects people over 60. It presents with widespread swollen nodes, fever, rash and immune upsets such as anaemia; about four in ten people are alive five years after chemotherapy, more after a transplant in first remission."},{"label":"Peripheral T-cell lymphomas","href":"/cancers/peripheral-t-cell-lymphoma/","tip":"Peripheral T-cell lymphomas are lymphomas of T cells rather than B cells. They are rarer, more varied and, apart from a few subtypes, harder to treat than B-cell lymphomas; several new drugs help only defined subtypes."},{"label":"Non-Hodgkin lymphoma","href":"/cancers/non-hodgkin-lymphoma/","tip":"Non-Hodgkin lymphoma is not one disease but a family of more than sixty cancers of the lymphocytes, the white blood cells of the immune system. About 95 per cent come from B cells and the rest from T or NK cells; some grow over years and are watched, others grow over weeks and are treated to cure. The family is the map; the subtype is the disease, and the subtype is what decides the treatment."}],"tags":[{"label":"lymphoma","href":"/tagged/lymphoma/","tip":"Every record tagged lymphoma."}]},"sortKeys":{"year":0}},{"id":"ros1-fusion","name":"ROS1 fusion (ROS1-positive)","tldr":"A ROS1 fusion drives about 1 to 2 percent of lung adenocarcinomas and behaves much like ALK. Crizotinib, entrectinib, repotrectinib and taletrectinib are approved for it.","route":"/biomarkers/ros1-fusion/","kind":"biomarker","target":{"id":"ros1","name":"ROS1","targetClass":"kinase","tldr":"A gene fusion in about 1-2% of lung cancers that responds for years to targeted pills, now in their third generation."},"sub":"ROS1","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"fusion","href":"/tagged/fusion/","tip":"Every record tagged fusion."}]},"sortKeys":{"year":0}},{"id":"rejuv-age-senescent-cells-after-treatment","name":"Senescent cells and p16 after chemotherapy","tldr":"Chemotherapy pushes cells into senescence: they stop dividing but stay alive and keep releasing inflammatory signals. The usual marker, p16INK4a in blood T cells, rises sharply during treatment and is still raised a year later. In one study the rise matched about fifteen years of ordinary ageing, in another the gap in survivors was larger still.","route":"/technologies/rejuv-age-senescent-cells-after-treatment/","status":"emerging","kind":"technology","schematic":{"id":"rejuv-age-senescent-cells-after-treatment","sections":["rejuvenation","supportive-care"]},"facets":{"kind":["Technology"],"cancers":[],"year":[]},"cols":{"kind":{"facet":"kind","value":"Technology","tip":"Every way we see, measure, or attack a tumour, explained."},"cancers":[],"tags":[{"label":"rejuvenation","href":"/tagged/rejuvenation/","tip":"Every record tagged rejuvenation."},{"label":"survivorship","href":"/tagged/survivorship/","tip":"Every record tagged survivorship."},{"label":"biological-ageing","href":"/tagged/biological-ageing/","tip":"Every record tagged biological-ageing."},{"label":"senescence","href":"/tagged/senescence/","tip":"Every record tagged senescence."}]},"sortKeys":{"year":0}},{"id":"sstr-pet-expression","name":"Somatostatin receptor expression by PET (SSTR-positive)","tldr":"Somatostatin receptor-positive means a neuroendocrine tumour takes up a DOTATATE tracer on PET. It is the requirement for lutetium-177 dotatate and the marker that predicts response to octreotide and lanreotide.","route":"/biomarkers/sstr-pet-expression/","kind":"biomarker","target":{"id":"sstr2","name":"Somatostatin receptor 2","targetClass":"surface-antigen","tldr":"Somatostatin receptor 2 is a hormone receptor densely present on neuroendocrine tumours, and was the first theranostic target to reach routine care."},"sub":"SSTR2","facets":{"kind":["Biomarker"],"cancers":["Neuroendocrine tumours","Pancreatic neuroendocrine tumours","Lung neuroendocrine tumours"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Neuroendocrine tumours","href":"/cancers/neuroendocrine/","tip":"A family of usually slow-growing tumours that start in hormone-producing cells of the gut, pancreas and lungs. They pioneered the idea of using the same molecule to see a tumour on a scan and then to treat it with radiation."},{"label":"Pancreatic neuroendocrine tumours","href":"/cancers/pancreatic-net/","tip":"Pancreatic neuroendocrine tumours arise from the hormone-producing islet cells of the pancreas and behave very differently from ordinary pancreatic cancer, often growing for years. Surgery cures localised tumours; advanced disease is treated in sequence with somatostatin analogues, lutetium-177 dotatate, targeted tablets and oral chemotherapy, and a minority secrete insulin or gastrin."},{"label":"Lung neuroendocrine tumours","href":"/cancers/lung-net/","tip":"Lung neuroendocrine tumours, called typical and atypical carcinoids, are slow-growing tumours of the airways that are usually cured by surgery. When they spread, everolimus is the one drug tested in a randomised trial for this site, cabozantinib was approved in 2025, and somatostatin analogues and lutetium radioligand therapy are borrowed from gut tumours."}],"tags":[{"label":"pet","href":"/tagged/pet/","tip":"Every record tagged pet."}]},"sortKeys":{"year":0}},{"id":"spop-mutation","name":"SPOP mutation","tldr":"The commonest single point mutation in prostate cancer, in about one tumour in eight. Tumours carrying it never have the usual ERG fusion, and men whose metastatic disease carries it tend to stay hormone-sensitive for longer.","route":"/biomarkers/spop-mutation/","kind":"biomarker","target":{"id":"spop","name":"SPOP","targetClass":"oncogene","tldr":"SPOP (Speckle-type POZ protein) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Prostate cancer, Endometrial cancer, Non-Hodgkin lymphoma and 4 more."},"sub":"SPOP","facets":{"kind":["Biomarker"],"cancers":["Prostate cancer","Metastatic hormone-sensitive prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Metastatic hormone-sensitive prostate cancer","href":"/cancers/prostate-mhspc/","tip":"Metastatic hormone-sensitive prostate cancer is disease that has spread but still responds to lowering testosterone. Hormone therapy alone is no longer enough: adding an androgen receptor inhibitor, and docetaxel for high-volume disease, lengthens life by years."}],"tags":[{"label":"prostate","href":"/tagged/prostate/","tip":"Every record tagged prostate."}]},"sortKeys":{"year":0}},{"id":"stk11-keap1-loss","name":"STK11 or KEAP1 loss in KRAS-mutant lung adenocarcinoma","tldr":"Two genes that, when broken in a lung cancer that also has a faulty KRAS gene, predict that immunotherapy will work much less well. In a lung cancer with a normal KRAS gene the same faults appear to make no difference.","route":"/biomarkers/stk11-keap1-loss/","kind":"biomarker","target":{"id":"stk11","name":"STK11","targetClass":"kinase","tldr":"STK11 is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response."},"sub":"STK11","facets":{"kind":["Biomarker"],"cancers":["Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."}],"tags":[{"label":"immunotherapy","href":"/tagged/immunotherapy/","tip":"Every record tagged immunotherapy."}]},"sortKeys":{"year":0}},{"id":"rejuv-age-telomere-length","name":"Telomere length after treatment","tldr":"Telomeres are the caps on chromosomes that shorten each time a cell divides. They are the oldest and best known measure of cellular ageing, and the one with the least to show for itself in cancer survivors so far: the measurements exist, the associations are inconsistent, and nothing follows from a result.","route":"/technologies/rejuv-age-telomere-length/","status":"emerging","kind":"technology","schematic":{"id":"rejuv-age-telomere-length","sections":["rejuvenation","supportive-care"]},"facets":{"kind":["Technology"],"cancers":[],"year":[]},"cols":{"kind":{"facet":"kind","value":"Technology","tip":"Every way we see, measure, or attack a tumour, explained."},"cancers":[],"tags":[{"label":"rejuvenation","href":"/tagged/rejuvenation/","tip":"Every record tagged rejuvenation."},{"label":"survivorship","href":"/tagged/survivorship/","tip":"Every record tagged survivorship."},{"label":"biological-ageing","href":"/tagged/biological-ageing/","tip":"Every record tagged biological-ageing."}]},"sortKeys":{"year":0}},{"id":"tissue-factor-expression","name":"Tissue factor expression","tldr":"Tissue factor, the clotting trigger, is overexpressed on cervical and several other cancers. Tisotumab vedotin is labelled for cervical cancer without a tissue factor test.","route":"/biomarkers/tissue-factor-expression/","kind":"biomarker","target":{"id":"tissue-factor","name":"Tissue factor","targetClass":"surface-antigen","tldr":"Tissue factor is a clotting protein that cancers abnormally display on their surface, used as an ADC target in cervical cancer."},"sub":"F3","facets":{"kind":["Biomarker"],"cancers":["Cervical cancer","Recurrent or metastatic cervical cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Cervical cancer","href":"/cancers/cervical/","tip":"A cancer that could be eliminated by HPV vaccination and screening. For those who develop it, immunotherapy and a tissue-factor ADC have improved survival."},{"label":"Recurrent or metastatic cervical cancer","href":"/cancers/recurrent-metastatic-cervical-cancer/","tip":"Recurrent or metastatic cervical cancer has spread beyond the pelvis or come back where it cannot be cured by surgery or radiotherapy. Pembrolizumab added to chemotherapy and bevacizumab is the first treatment, and the antibody-drug conjugate tisotumab vedotin or the PD-1 antibody cemiplimab extend life when it progresses."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"tmb-high","name":"TMB-high (tumour mutational burden >= 10 mutations per megabase)","tldr":"TMB counts how many mutations a tumour carries per million DNA letters. Ten or more, measured by FoundationOne CDx, allows pembrolizumab for almost any solid tumour after other treatment has failed.","route":"/biomarkers/tmb-high/","kind":"biomarker","sub":"Genome-wide readout","facets":{"kind":["Biomarker"],"cancers":["Metastatic cancer","Non-small-cell lung cancer","Melanoma","Bladder & urothelial cancer","Triple-negative breast cancer","Metastatic triple-negative breast cancer","Pancreatic ductal adenocarcinoma","Colorectal cancer","Gallbladder cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Metastatic cancer","href":"/cancers/metastatic-cancer/","tip":"Metastatic cancer means the original cancer has spread to other parts of the body, most often the bones, liver, lungs or brain. It keeps the name of where it started, is treated with therapies that reach the whole body, and can increasingly be controlled for years; with limited spread it is sometimes treated with the aim of cure."},{"label":"Non-small-cell lung cancer","href":"/cancers/nsclc/","tip":"Non-small-cell lung cancer is the proving ground for precision medicine: a dozen targetable mutations each with a matched pill, immunotherapy for the rest, and ADCs and bispecifics arriving now. Because most cases are still found late, low-dose CT screening is the other half of the story."},{"label":"Melanoma","href":"/cancers/melanoma/","tip":"The skin cancer that proved immunotherapy works: half of advanced patients now live 10 years. Also the first with an approved TIL therapy, an oncolytic virus, and a positive phase 3 personalised vaccine."},{"label":"Bladder & urothelial cancer","href":"/cancers/urothelial/","tip":"Bladder cancer went from 40 years of cisplatin to an ADC-immunotherapy combination that nearly doubled survival, and in 2026 the first blood-test-guided drug approval."}],"tags":[{"label":"genome-wide","href":"/tagged/genome-wide/","tip":"Every record tagged genome-wide."}]},"sortKeys":{"year":0}},{"id":"tmprss2-erg-fusion","name":"TMPRSS2-ERG fusion (and the other ETS rearrangements)","tldr":"The commonest genetic change in prostate cancer, present in roughly half of tumours. Nothing treats it and it does not make the cancer more dangerous; it is useful mainly for recognising that two samples came from the same tumour.","route":"/biomarkers/tmprss2-erg-fusion/","kind":"biomarker","target":{"id":"erg","name":"ERG","targetClass":"oncogene","tldr":"ERG (Transcriptional regulator ERG) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Sarcomas, Prostate cancer, Non-Hodgkin lymphoma and 4 more."},"sub":"ERG","facets":{"kind":["Biomarker"],"cancers":["Prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."}],"tags":[{"label":"prostate","href":"/tagged/prostate/","tip":"Every record tagged prostate."}]},"sortKeys":{"year":0}},{"id":"tp53-del17p","name":"TP53 mutation and del(17p)","tldr":"TP53 mutation, or deletion of the 17p arm that carries the gene, is the single most common change in cancer and carries a worse outlook almost everywhere. In chronic lymphocytic leukaemia it decides treatment: chemotherapy is avoided and venetoclax's first approval was for del(17p) disease.","route":"/biomarkers/tp53-del17p/","kind":"biomarker","target":{"id":"tp53","name":"TP53","targetClass":"tumor-suppressor","tldr":"TP53 is the 'guardian of the genome', broken in half of all cancers. Fixing it directly has so far defeated every attempt, so drugs exploit what its loss makes cancers depend on."},"sub":"TP53","facets":{"kind":["Biomarker"],"cancers":["Chronic lymphocytic leukaemia","Relapsed or refractory chronic lymphocytic leukaemia","Acute myeloid leukaemia","Myelodysplastic syndromes / neoplasms","Endometrial cancer","p53-abnormal endometrial cancer, including uterine serous carcinoma","Triple-negative breast cancer","Ovarian cancer","Mantle cell lymphoma","Richter transformation of chronic lymphocytic leukaemia","Diffuse large B-cell lymphoma","Non-Hodgkin lymphoma"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Chronic lymphocytic leukaemia","href":"/cancers/cll/","tip":"A slow leukaemia that no longer needs chemotherapy: BTK inhibitors and venetoclax control it for years, often in fixed-duration courses."},{"label":"Relapsed or refractory chronic lymphocytic leukaemia","href":"/cancers/cll-relapsed/","tip":"When chronic lymphocytic leukaemia returns, the usual move is to switch drug class: venetoclax-based therapy after a BTK inhibitor, or a BTK inhibitor after venetoclax. Pirtobrutinib (BRUIN) works after the older BTK inhibitors fail, and CAR-T is approved for patients who have run out of both classes."},{"label":"Acute myeloid leukaemia","href":"/cancers/aml/","tip":"Acute myeloid leukaemia is an aggressive blood cancer where, after 40 years of the same chemotherapy, a wave of targeted drugs (FLT3, IDH, BCL-2, menin) arrived."},{"label":"Myelodysplastic syndromes / neoplasms","href":"/cancers/mds/","tip":"Bone-marrow disorders where blood cells are made badly and too few reach the blood; a third progress to acute leukaemia. Treatment ranges from transfusions and growth factors to hypomethylating drugs and, for the fit, transplant."}],"tags":[{"label":"tp53","href":"/tagged/tp53/","tip":"Every record tagged tp53."}]},"sortKeys":{"year":0}},{"id":"nepc-transformation","name":"Treatment-emergent neuroendocrine transformation (recognising it)","tldr":"The test result that shows a prostate cancer has changed into a different, faster kind of cancer under hormone treatment. It is made on a biopsy, usually prompted by disease that is growing while the PSA stays flat.","route":"/biomarkers/nepc-transformation/","kind":"biomarker","sub":"Genome-wide readout","facets":{"kind":["Biomarker"],"cancers":["Prostate cancer","Metastatic castration-resistant prostate cancer","Neuroendocrine and small-cell prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Prostate cancer","href":"/cancers/prostate/","tip":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype."},{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."},{"label":"Neuroendocrine and small-cell prostate cancer","href":"/cancers/prostate-nepc/","tip":"Neuroendocrine prostate cancer is a form that has stopped depending on the androgen receptor, either from the start or after years of hormone therapy. It no longer shows up on PSA, spreads to the liver and brain, and is treated with the platinum chemotherapy used for small-cell lung cancer."}],"tags":[{"label":"resistance","href":"/tagged/resistance/","tip":"Every record tagged resistance."}]},"sortKeys":{"year":0}},{"id":"trop2-expression","name":"TROP2 expression","tldr":"TROP2 is on the surface of most breast and lung cancers. Sacituzumab govitecan and datopotamab deruxtecan are given without measuring it; a computational TROP2 score is being tested as a selector in lung cancer.","route":"/biomarkers/trop2-expression/","kind":"biomarker","target":{"id":"trop2","name":"TROP2","targetClass":"surface-antigen","tldr":"TROP2 is a surface glycoprotein present at high levels on most epithelial cancers (breast, lung, urothelial, gastric, pancreatic) and at low levels on normal tissue. It does not drive the cancer; it is a delivery address, used by the approved ADCs sacituzumab govitecan and datopotamab deruxtecan and by sacituzumab tirumotecan, with a TROP2 PET tracer in development to pick patients."},"sub":"TACSTD2","facets":{"kind":["Biomarker"],"cancers":["Triple-negative breast cancer","Metastatic triple-negative breast cancer","HR-positive / HER2-negative breast cancer","Bladder & urothelial cancer","Non-small-cell lung cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Triple-negative breast cancer","href":"/cancers/tnbc/","tip":"A breast cancer that lacks the three receptors (oestrogen, progesterone, HER2) that other breast cancers can be treated through. It was the hardest subtype for decades; since 2020 immunotherapy and ADCs have changed that."},{"label":"Metastatic triple-negative breast cancer","href":"/cancers/tnbc-metastatic/","tip":"The treatment of triple-negative breast cancer that has spread has been transformed since 2020, though it is not yet curable. By PD-L1 score, first treatment is pembrolizumab with chemotherapy or with sacituzumab govitecan, or datopotamab deruxtecan or sacituzumab govitecan alone; BRCA carriers can take a PARP inhibitor tablet; and trastuzumab deruxtecan reaches the third of tumours with low HER2."},{"label":"HR-positive / HER2-negative breast cancer","href":"/cancers/breast-hr-positive/","tip":"HR-positive breast cancer is the most common breast cancer, driven by oestrogen. It was treated for years with hormone-blocking pills, now joined by CDK4/6 inhibitors, PI3K-pathway drugs, degraders, and ADCs."},{"label":"Bladder & urothelial cancer","href":"/cancers/urothelial/","tip":"Bladder cancer went from 40 years of cisplatin to an ADC-immunotherapy combination that nearly doubled survival, and in 2026 the first blood-test-guided drug approval."}],"tags":[{"label":"surface-antigen","href":"/tagged/surface-antigen/","tip":"Every record tagged surface-antigen."},{"label":"no-threshold","href":"/tagged/no-threshold/","tip":"Every record tagged no-threshold."}]},"sortKeys":{"year":0}},{"id":"brca-somatic","name":"Tumour (somatic or germline) BRCA1/2 mutation and HRR gene alterations","tldr":"Tumour BRCA testing finds BRCA1/2 mutations in the cancer itself, whether inherited or acquired; wider panels add other repair genes such as ATM and PALB2. Ovarian and prostate cancer labels accept the tumour result for PARP inhibitors.","route":"/biomarkers/brca-somatic/","kind":"biomarker","target":{"id":"brca","name":"BRCA1 / BRCA2 (HRD)","targetClass":"tumor-suppressor","tldr":"DNA repair genes. Inheriting a broken copy raises breast and ovarian cancer risk, but tumours that lose them become uniquely vulnerable to PARP inhibitors and platinum."},"sub":"BRCA1, BRCA2","facets":{"kind":["Biomarker"],"cancers":["Ovarian cancer","High-grade serous ovarian cancer","Platinum-sensitive ovarian cancer","Metastatic castration-resistant prostate cancer","Triple-negative breast cancer","Pancreatic ductal adenocarcinoma","BRCA or PALB2-mutant pancreatic ductal adenocarcinoma","Prostate cancer"],"year":[]},"cols":{"kind":{"facet":"kind","value":"Biomarker","tip":"The readouts a pathology report gives (PD-L1 CPS, HER2 IHC 3+, MSI-high), each under its gene or protein, with the thresholds approvals use and the tests that measure them."},"cancers":[{"label":"Ovarian cancer","href":"/cancers/ovarian/","tip":"Usually found late. PARP inhibitors transformed maintenance therapy, and ADCs against folate receptor and CDH6 are arriving for platinum-resistant disease."},{"label":"High-grade serous ovarian cancer","href":"/cancers/high-grade-serous-ovarian-cancer/","tip":"High-grade serous cancer is the common, aggressive form of ovarian cancer, now known to start in the fallopian tube. It is treated with surgery and platinum chemotherapy, and maintenance PARP inhibitors have changed its course for the half of patients whose tumours cannot repair DNA properly."},{"label":"Platinum-sensitive ovarian cancer","href":"/cancers/platinum-sensitive-ovarian-cancer/","tip":"Platinum-sensitive ovarian cancer is disease that responded to carboplatin and either has not relapsed or relapses more than six months after the last dose. It is treated with further platinum chemotherapy, sometimes repeat surgery, and above all with maintenance PARP inhibitors, which keep BRCA-mutant tumours away for years and have raised long-term survival."},{"label":"Metastatic castration-resistant prostate cancer","href":"/cancers/prostate-mcrpc/","tip":"Metastatic castration-resistant prostate cancer is disease that grows despite castrate testosterone. Sequenced treatments now include androgen receptor inhibitors, docetaxel and cabazitaxel, PARP inhibitors for men with BRCA-type mutations, the radioligand 177Lu-PSMA-617 and radium-223 for bone-predominant disease."}],"tags":[{"label":"brca","href":"/tagged/brca/","tip":"Every record tagged brca."}]},"sortKeys":{"year":0}}]