{"entity":{"id":"non-hodgkin-lymphoma","kind":"cancer","name":"Non-Hodgkin lymphoma (all types)","aka":["Non-Hodgkin Lymphoma","NHL","Non-Hodgkin's lymphoma","Lymphoma (non-Hodgkin)","Lymphoma","Mature B-cell neoplasms","Mature T-cell and NK-cell neoplasms","B-cell lymphoma","T-cell lymphoma","NK-cell lymphoma","Lymphatic cancer","Cancer of the lymph glands","C82","C83","C84","C85","C86"],"tldr":"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.","summary":"What it is. Non-Hodgkin lymphoma is not a disease. It is the name given to every cancer of the lymphatic system that is not Hodgkin lymphoma, and it covers scores of separate diseases whose only shared feature is the cell they come from: the tables of the 2022 WHO classification list more than sixty mature B-cell, T-cell and NK-cell entities: a lymphocyte, one of the white blood cells that run the immune system. Two people both told they have non-Hodgkin lymphoma may have conditions that differ more from each other than breast cancer differs from bowel cancer. One may be watched for ten years without treatment; the other may start chemotherapy the week of diagnosis with the intention of cure. The single most useful thing to find out after the word lymphoma is the rest of the name on the report, because that is what decides everything.\n\nHow the classification is built, in plain words. The reference book is the fifth edition of the World Health Organization Classification of Haematolymphoid Tumours, published in 2022 and usually shortened to WHO-HAEM5. It does not use the phrase non-Hodgkin lymphoma at all. It sorts lymphomas on a tree: first by the class of cell, then into a family of related diseases, then into the entity that is the diagnosis. The first fork is B-cell on one side and T-cell and NK-cell on the other. B cells make antibodies; T cells and NK cells kill infected cells directly. In the United Kingdom the B-cell side is about 95 per cent of lymphoma diagnoses and the T-cell and NK-cell side about 5 per cent (Haematological Malignancy Research Network, 5,796 lymphomas in a population of nearly four million). That first fork matters because B cells carry a protein called CD20 on their surface and T cells do not, and the antibody that attaches to CD20, rituximab, is the drug that transformed B-cell lymphoma from 1997 onwards and has no equivalent on the T-cell side.\n\nThe second thing a reader is told is the pace, and it is the fork that decides what happens next week. Indolent lymphomas grow over years: follicular lymphoma, marginal zone lymphoma, lymphoplasmacytic lymphoma, most cutaneous T-cell lymphoma. They are generally not curable with the treatments in use today, and they are also not usually urgent, so a person with no symptoms may reasonably be watched rather than treated, sometimes for a decade. Aggressive lymphomas grow over weeks: diffuse large B-cell lymphoma, high-grade B-cell lymphoma, Burkitt lymphoma, most of the T-cell lymphomas. They are treated immediately and they are treated to cure. The sentence that surprises people most is that the aggressive ones are the ones more often cured, and the slow ones the ones more often lived with. Waiting is not neglect in an indolent lymphoma; it is the treatment that has been shown not to shorten life, and the glossary entry on watching and waiting says what is being watched for.\n\nThe third fork is where the lymphoma is. Nodal lymphoma arises in lymph nodes, the bean-sized filters strung along the lymphatic vessels, and shows itself as a painless lump in the neck, armpit or groin. Extranodal lymphoma arises in an organ that has lymphoid tissue in it but is not a lymph node: the stomach, the eye socket, the skin, the brain, the testis, the small bowel, the thyroid, the salivary gland. A substantial minority of non-Hodgkin lymphomas start outside the lymph nodes, and the site changes the disease. A marginal zone lymphoma in the stomach is usually caused by a bacterial infection and is usually cured by a fortnight of antibiotics; the same cell type in a lymph node is not. A large B-cell lymphoma in the testis, the eye or the brain behaves as one disease across those three sites, which WHO-HAEM5 recognised in 2022 by grouping them as lymphomas of immune-privileged sites, places the immune system does not patrol.\n\nWho gets it. Lymphoma is mostly a disease of later life: the median age at diagnosis in the HMRN population was 67.2 years for all lymphomas together and 69.1 years for the non-Hodgkin group, with men diagnosed younger than women and at higher rates at almost every age. But the family spans every age, and different subtypes dominate different ages: Burkitt lymphoma and Hodgkin lymphoma are the common lymphomas of childhood and early adult life, while above 60 the diffuse large B-cell, marginal zone and follicular subtypes account for more than 80 per cent of diagnoses. Most people with lymphoma have no identifiable cause. The known causes account for a minority and are worth naming because several are preventable or treatable: Epstein-Barr virus, the virus of glandular fever, which is involved in Burkitt lymphoma, in some diffuse large B-cell lymphomas and in extranodal NK/T-cell lymphoma; Helicobacter pylori in the stomach; hepatitis C; HIV; HTLV-1, which causes adult T-cell leukaemia/lymphoma; Kaposi sarcoma herpesvirus, which causes primary effusion lymphoma; coeliac disease, which precedes enteropathy-associated T-cell lymphoma; immune suppression after an organ transplant; and autoimmune diseases such as Sjogren syndrome and Hashimoto thyroiditis, which produce the lymphoid tissue that marginal zone lymphomas grow in. Cancer Research UK estimates that about 3 per cent of UK cases are preventable, which is the honest counterpart to the fact that most people did nothing to cause this.\n\nHow it is staged, and why the old words survive. Lymphoma is not staged with the TNM system used for solid tumours, because it does not have a primary tumour and lymph nodes in the way a breast or bowel cancer does: in lymphoma, the lymph nodes are the disease. The system in use is the Lugano classification, agreed at the International Conference on Malignant Lymphoma in Lugano in 2011 and published in 2014. It counts how many regions of lymph nodes are involved and whether they sit on one side of the diaphragm or both: stage I is one region, stage II is two or more on the same side, stage III is both sides, stage IV is disease that has spread diffusely into an organ such as the bone marrow, liver or lung. Lugano kept the descriptive language of the Ann Arbor system that preceded it, agreed at a meeting in Ann Arbor, Michigan in 1971 for Hodgkin's disease, which is why a report in 2026 may still say Ann Arbor stage IIA and mean the same thing. What Lugano changed is how the stage is measured: PET-CT scanning became the standard staging test for the lymphomas that take up the tracer, the A and B suffixes for fever, night sweats and weight loss are now recorded only for Hodgkin lymphoma, and a routine bone marrow biopsy is no longer needed to stage Hodgkin lymphoma or, in most cases, diffuse large B-cell lymphoma.\n\nStage is not the main thing. This is the largest difference between lymphoma and the cancers most people have heard of. In breast or bowel cancer the stage is the dominant fact; in lymphoma the subtype matters more, and within a subtype the prognosis is read from a score that counts clinical features rather than anatomy. The International Prognostic Index, built in 1993 from 2,031 patients with aggressive lymphoma treated across 16 institutions, counts five: age over 60, stage III or IV, a raised lactate dehydrogenase, a performance status of 2 or worse, and more than one site outside the lymph nodes. Follicular lymphoma has its own version (FLIPI), mantle cell lymphoma has MIPI, and the nodal T-cell lymphomas have the Prognostic Index for T-cell lymphoma, built from 385 patients in 2004. Stage IV lymphoma is a routine curable diagnosis, which is the opposite of what the word means in most other cancers, and it is worth saying out loud at the point where somebody has just been handed the number.\n\nThe state of the art, in one paragraph. The B-cell side has had thirty years of advances that compound. Rituximab, approved in 1997, was the first antibody ever licensed for a cancer, and adding it to chemotherapy raised both the proportion of people whose diffuse large B-cell lymphoma went away and the proportion still alive years later; the trial and its figures are on that page. CAR-T cell therapy, in which a patient's own T cells are collected, engineered to recognise CD19 and given back, was approved for relapsed large B-cell lymphoma in 2017 and now cures a proportion of people whose disease had come back after chemotherapy. Bispecific antibodies, which grip a lymphoma cell with one arm and a T cell with the other, arrived in 2023 and do a related job without the manufacturing wait. Antibody-drug conjugates deliver chemotherapy to the cell that carries a particular marker. The T-cell and NK-cell side has had almost none of this: there is no CD20 to aim at, the entities are individually rare, and brentuximab vedotin added to chemotherapy for CD30-positive disease is the only randomised first-line advance in twenty years. The gap between the two sides of the first fork is the largest unsolved problem in this family, and it is a gap in research effort as much as in biology.\n\nA note on names. Because two classifications were published in 2022 and they do not agree about everything, a British report, an American report and a trial protocol may give the same disease three names. Where that happens the pages in this family give both and say which book each name comes from. The glossary entry on the two classifications lists the disagreements that change what a patient is called.","asOf":"2026-09-29","wikipedia":"https://en.wikipedia.org/wiki/Non-Hodgkin_lymphoma","links":[{"label":"NCI: Lymphoma","url":"https://www.cancer.gov/types/lymphoma"},{"label":"GLOBOCAN 2020 (Sung 2021)","url":"https://doi.org/10.3322/caac.21660"},{"label":"Lymphoma Action: helpline services","url":"https://lymphoma-action.org.uk/information-and-support/support-you/helpline-services"},{"label":"Lymphoma Action: questions to ask your medical team about lymphoma","url":"https://lymphoma-action.org.uk/information-and-support/tests-scans-and-lymphoma-staging/questions-ask-your-medical-team-about-lymphoma"},{"label":"Lymphoma Action: follow-up after lymphoma treatment","url":"https://lymphoma-action.org.uk/information-and-support/living-and-beyond-lymphoma/follow-after-lymphoma-treatment"},{"label":"Lymphoma Action: infections, risk and prevention","url":"https://lymphoma-action.org.uk/information-and-support/side-effects-lymphoma-and-treatment/infections-risk-and-prevention"},{"label":"Lymphoma Action: neutropenia (low neutrophils)","url":"https://lymphoma-action.org.uk/information-and-support/side-effects-lymphoma-and-treatment/neutropenia-low-neutrophils"},{"label":"Lymphoma Action: cancer-related fatigue","url":"https://lymphoma-action.org.uk/information-and-support/side-effects-lymphoma-and-treatment/cancer-related-fatigue"},{"label":"Lymphoma Action: lymphoma, work and you","url":"https://lymphoma-action.org.uk/information-and-support/living-and-beyond-lymphoma/day-day-living/lymphoma-work-and-you"},{"label":"Maggie's: support and information","url":"https://www.maggies.org/support-and-information/"},{"label":"NHS: non-Hodgkin lymphoma","url":"https://www.nhs.uk/conditions/non-hodgkin-lymphoma/"},{"label":"NHS: non-Hodgkin lymphoma, 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and management","url":"https://www.nice.org.uk/guidance/ng52"},{"label":"NICE NG47: haematological cancers, improving outcomes","url":"https://www.nice.org.uk/guidance/ng47"},{"label":"Lymphoma Action: lymphoma staging","url":"https://lymphoma-action.org.uk/information-and-support/tests-scans-and-lymphoma-staging/lymphoma-staging"},{"label":"Lymphoma Action: biopsy","url":"https://lymphoma-action.org.uk/information-and-support/tests-scans-and-lymphoma-staging/biopsy"},{"label":"Lymphoma Action: CT and PET/CT scans","url":"https://lymphoma-action.org.uk/information-and-support/tests-scans-and-lymphoma-staging/ct-and-petct-scan"},{"label":"Lymphoma Action: waiting for test and scan results","url":"https://lymphoma-action.org.uk/information-and-support/tests-scans-and-lymphoma-staging/waiting-test-and-scan-results"},{"label":"Lymphoma Action: your medical team","url":"https://lymphoma-action.org.uk/information-and-support/tests-scans-and-lymphoma-staging/your-medical-team-mdt"},{"label":"Lymphoma Action: taking part in a clinical trial","url":"https://lymphoma-action.org.uk/information-and-support/lymphoma-treatment/clinical-trials-lymphoma-trialslink/taking-part-clinical"},{"label":"Lymphoma Action: caring for someone who has lymphoma","url":"https://lymphoma-action.org.uk/information-and-support/relationships-family-friends/caring-someone-who-has-lymphoma"},{"label":"NHS: carer's assessments","url":"https://www.nhs.uk/social-care-and-support/support-and-benefits-for-carers/carer-assessments/"},{"label":"NHS: when to use 111","url":"https://www.nhs.uk/nhs-services/urgent-and-emergency-care-services/when-to-use-111/"},{"label":"NHS: when to call 999","url":"https://www.nhs.uk/nhs-services/urgent-and-emergency-care-services/when-to-call-999/"},{"label":"NHS: sepsis","url":"https://www.nhs.uk/conditions/sepsis/"},{"label":"Macmillan: metastatic spinal cord compression","url":"https://www.macmillan.org.uk/cancer-information-and-support/impacts-of-cancer/metastatic-spinal-cord-compression"},{"label":"Macmillan: superior vena cava obstruction","url":"https://www.macmillan.org.uk/cancer-information-and-support/impacts-of-cancer/superior-vena-cava-obstruction"},{"label":"NICE NG234: spinal metastases and metastatic spinal cord compression","url":"https://www.nice.org.uk/guidance/ng234"},{"label":"WHO Classification of Haematolymphoid Tumours, 5th edition: lymphoid neoplasms (Alaggio, Leukemia 2022)","url":"https://doi.org/10.1038/s41375-022-01620-2"},{"label":"International Consensus Classification of Mature Lymphoid Neoplasms (Campo, Blood 2022)","url":"https://doi.org/10.1182/blood.2022015851"},{"label":"Lymphoma incidence, survival and prevalence 2004 to 2014, subtype analyses from the UK Haematological Malignancy Research Network (Smith, Br J Cancer 2015)","url":"https://doi.org/10.1038/bjc.2015.94"},{"label":"Lugano classification: recommendations for initial evaluation, staging and response assessment of Hodgkin and non-Hodgkin lymphoma (Cheson, J Clin Oncol 2014)","url":"https://doi.org/10.1200/JCO.2013.54.8800"},{"label":"SEER Cancer Stat Facts: non-Hodgkin lymphoma (United States incidence, mortality and relative survival)","url":"https://seer.cancer.gov/statfacts/html/nhl.html"},{"label":"Cancer Research UK: non-Hodgkin lymphoma statistics (incidence, mortality, survival)","url":"https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/non-hodgkin-lymphoma"},{"label":"NCI PDQ: adult non-Hodgkin lymphoma treatment (health professional version)","url":"https://www.cancer.gov/types/lymphoma/hp/adult-nhl-treatment-pdq"},{"label":"NCI PDQ: adult non-Hodgkin lymphoma treatment (patient version)","url":"https://www.cancer.gov/types/lymphoma/patient/adult-nhl-treatment-pdq"},{"label":"Lymphoma Action: types of lymphoma (UK patient charity)","url":"https://lymphoma-action.org.uk/types-lymphoma"},{"label":"Lymphoma Research Foundation: about lymphoma","url":"https://lymphoma.org/understanding-lymphoma/aboutlymphoma/"},{"label":"GLOBOCAN 2020 global cancer statistics (Sung, CA Cancer J Clin 2021)","url":"https://doi.org/10.3322/caac.21660"},{"label":"NICE NG12: suspected cancer, haematological cancers (1.10.1 to 1.10.9)","url":"https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer"},{"label":"Lymphoma Action: the UK lymphoma charity","url":"https://lymphoma-action.org.uk/"},{"label":"Cancer Research UK: non-Hodgkin lymphoma 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with non-Hodgkin lymphoma, the decisions and the people who make them: This is orientation from public patient pages, guidelines and the trials themselves, not advice for your case: your own team's instructions and the 24-hour number they gave you come first, and no figure here is a prediction about you. The decision records, the question sets, the first 60 days checklist and the red cards on this page were written from the NHS, Lymphoma Action, Macmillan and Cancer Research UK patient pages, from NICE NG52, NG47, CG151 and NG234, from the NHS Breast Screening Programme protocols and the Green Book, and from the trial reports named beside each figure, all read on 1 October 2026.","The biology in detail, 1 of 5. The antigens. Ten surface targets carry the lymphoma medicines, and nine of the ten are normal proteins on normal cells. CD20 and CD19 are B-cell lineage antigens, so anti-CD20 and anti-CD19 treatments empty the B-cell compartment and leave hypogammaglobulinaemia, more infection, a blunted vaccine response and a risk of hepatitis B reactivation; after CAR-T the aplasia is deeper and can last years. CD79b and CD22 are also B-cell antigens, chosen for conjugates because they internalise. CD30 is the nearest to a restricted antigen, carried by activated lymphocytes and monocytes but not by resting ones, which is why brentuximab vedotin's limiting toxicity is the auristatin payload rather than the target. CD38 is mostly a myeloma antigen with no lymphoma approval and one laboratory consequence worth knowing, a positive indirect antiglobulin test that masks alloantibodies. CD47 is on every red cell, so blocking it causes anaemia by design and the dosing had to be redesigned around that. CCR4 is on regulatory T cells as well as on cutaneous and adult T-cell lymphoma, so depleting it causes rash and raises transplant risk. CD52 is on B cells, T cells, monocytes and dendritic cells at very high density, which makes alemtuzumab efficient and leaves CD4 counts low for a year. CD3 is the one target not on the tumour at all in B-cell disease: it is the handle a bispecific antibody grips, and cytokine release syndrome is that mechanism working.","The biology in detail, 2 of 5. The lesions. Chronic active B-cell receptor signalling defines the activated B-cell-like group and was shown by killing those cells, and only those cells, with knockdown of IgM, CD79A, CD79B or BTK; CD79B ITAM mutations were present in 18% of them and activating CARD11 mutations in about 10%. MYD88 L265P feeds the same NF-kB hub from the toll-like receptor side in 29% of activated B-cell-like cases, 9% of MALT lymphomas and 91% of lymphoplasmacytic lymphoma. BCL2 arrives by a recombinase error at the pre-B-cell stage, t(14;18), present in most follicular lymphomas and 13.5% of unselected large B-cell lymphomas. MYC arrives the same way in Burkitt lymphoma, where it needs a partner that supplies survival: TCF3 or ID3 mutation in 70% of sporadic cases and CCND3 mutation in 38%. BCL6 is rearranged in 28.7% of large B-cell lymphomas. EZH2 Tyr646 substitutions, 7.2% of follicular and 21.7% of germinal-centre large B-cell lymphoma, are gain-of-function and absent from the activated subtype. CREBBP or EP300 inactivation affects about 39% and 41%, and KMT2D 32% and 89%. TP53 loss is the commonest route out of chemotherapy sensitivity, 11% in mantle cell lymphoma with median overall survival of 1.8 years against 12.7, and 47.1% in Richter transformation.","The biology in detail, 3 of 5. The immune lesions and the viruses. Classical Hodgkin lymphoma and primary mediastinal B-cell lymphoma amplify 9p24.1, which carries both PD-1 ligand genes and JAK2; 97% of 108 classical Hodgkin lymphomas had concordant alterations of the two ligand loci, and CIITA, the master regulator of MHC class II, is rearranged in 38% of mediastinal and 15% of Hodgkin cases. That is why PD-1 blockade produced responses in 20 of 23 heavily pre-treated Hodgkin patients and does very little elsewhere in B-cell lymphoma. The Hodgkin node is mostly not cancer: the Reed-Sternberg cells are a small minority, their clonal B-cell identity had to be proved by picking single cells off a slide with a micromanipulator, and the infiltrate carries prognostic information of its own, with more CD68-positive macrophages predicting worse outcome. Two viruses matter. Epstein-Barr virus persists in almost everyone and causes different lymphomas according to which latency programme the infected cell runs: EBNA1 alone in Burkitt lymphoma, LMP1 added in Hodgkin and NK/T-cell lymphoma, and the full set where T-cell surveillance has gone. HTLV-1 starts adult T-cell leukaemia/lymphoma with Tax and HBZ, and the 426-case genomic analysis showed the acquired mutations cluster in the pathways Tax itself touches.","The biology in detail, 4 of 5. Resistance. Anti-CD20 fails by transcriptional down-regulation of CD20, found in 5 of 19 rebiopsied relapses, and by trogocytosis, in which macrophages shave the antigen off a living cell. Covalent BTK inhibitors fail on-target through BTK C481S, found in five of six patients with acquired resistance, which is answered by a non-covalent inhibitor giving 73.3% responses after a covalent one; they also fail through gain-of-function PLCG2 mutations below the kinase, which no BTK inhibitor reaches. Non-covalent inhibitors are in turn defeated by L528W and T474I, and L528W is enriched after zanubrutinib specifically, 7 of 13 progressing patients against 1 of 24 after ibrutinib. Venetoclax fails through BCL2 G101V in its own binding groove, which lowers affinity about 180-fold, appeared in 7 of 15 paired patients and is detectable months before progression. CD19 CAR-T fails through antigen loss by deletion, exon 2 mutation or exon 2 skipping, through the fitness of the collected T cells, where memory signatures predict response and exhaustion signatures predict failure, and through the node itself. Checkpoint blockade in Hodgkin lymphoma fails with loss of MHC class II, not class I, which is what points at a CD4 T cell as the effector.","The biology in detail, 5 of 5. The tests. An excisional biopsy rather than a core where it is possible, because architecture decides several of these diagnoses and because in Hodgkin lymphoma the malignant cells are rare enough to be missed. An immunohistochemistry panel of 10 to 12 stains, from which the Hans algorithm reads cell of origin. FISH for MYC, with BCL2 and BCL6 where MYC is rearranged or MYC protein is high, for CCND1 in a suspected mantle cell lymphoma, for t(11;18) in a gastric MALT lymphoma before relying on Helicobacter eradication, and for 9p24.1 where a research question needs it. Flow cytometry where cells can be put in suspension, which is how Sezary cells are counted and marrow involvement measured. Immunoglobulin and T-cell receptor clonality where the morphology is equivocal, remembering that clonality is not malignancy. A sequencing panel where TP53, MYD88, CXCR4, EZH2, BTK, PLCG2, BCL2 or the T-follicular-helper genes would change the plan. And FDG-PET, scored 1 to 5 against the mediastinal blood pool and the liver, which is the measurement lymphoma treatment is actually adapted to, with the warning that a score of 3 means different things in different protocols."],"group":"haematologic","burden":"About 13,747 new cases and 5,100 deaths a year in the United Kingdom, where 64.6 per cent of people are alive ten years later (Cancer Research UK); an estimated 79,320 new cases and 19,970 deaths in the United States in 2026, 3.8 per cent of all new cancer diagnoses, with five-year relative survival of 74.3 per cent for 2016 to 2022 (SEER); and about 544,000 cases and 260,000 deaths worldwide in 2020 (GLOBOCAN). It is the commonest group of blood cancers.","subtypes":["Diffuse large B-cell lymphoma","Follicular lymphoma","Marginal zone lymphoma","Mantle cell lymphoma","Chronic lymphocytic leukaemia / small lymphocytic lymphoma","Burkitt lymphoma","Waldenström macroglobulinaemia (lymphoplasmacytic lymphoma)","Primary CNS lymphoma","Peripheral T-cell lymphomas","Cutaneous T-cell lymphomas","HIV-associated lymphomas","B-cell lymphomas, about 95 per cent of lymphoma in the United Kingdom (HMRN)","Diffuse large B-cell lymphoma, the commonest single subtype at about 41 per cent of lymphoma diagnoses","Follicular lymphoma and the other indolent germinal-centre lymphomas","Marginal zone lymphomas: extranodal (MALT), nodal and splenic","Burkitt lymphoma and the high-grade B-cell lymphomas, including those with MYC and BCL2 rearrangements","Lymphoplasmacytic lymphoma, of which Waldenstrom macroglobulinaemia is the IgM type","Large B-cell lymphomas of immune-privileged sites: the central nervous system, the vitreoretina and the testis","Virus-associated B-cell lymphomas: EBV-positive, KSHV/HHV8-associated (primary effusion lymphoma) and plasmablastic lymphoma","Lymphomas arising in immune deficiency and dysregulation, including after transplant and in HIV","T-cell and NK-cell lymphomas, about 5 per cent of lymphoma in the United Kingdom","Nodal T-follicular helper cell lymphomas, of which the angioimmunoblastic type is the commonest","The anaplastic large cell lymphomas: ALK-positive, ALK-negative, primary cutaneous and breast implant-associated","Primary cutaneous T-cell lymphomas, of which mycosis fungoides is the commonest","EBV-positive NK/T-cell lymphomas, including extranodal NK/T-cell lymphoma","Adult T-cell leukaemia/lymphoma, caused by HTLV-1","Intestinal T-cell lymphomas: enteropathy-associated and monomorphic epitheliotropic"],"biomarkers":["Immunophenotype (CD20, CD5, CD10, CD30 and others) that assigns the subtype","MYC, BCL2 and BCL6 rearrangements (high-grade B-cell lymphoma)","Ki-67 proliferation index","Interim and end-of-treatment PET (Deauville score)","Cell of origin (germinal centre versus activated B-cell) in DLBCL","Cell of origin in large B-cell lymphoma: germinal-centre-like or non-germinal-centre, by the Hans three-stain algorithm or by expression profiling","MYC, BCL2 and BCL6 rearrangement by FISH: 8.8%, 13.5% and 28.7% of 442 unselected diffuse large B-cell lymphomas","MYD88 L265P: 29% of activated B-cell-like diffuse large B-cell lymphoma, 91% of lymphoplasmacytic lymphoma","CD79B ITAM mutation: 18% of activated B-cell-like diffuse large B-cell lymphoma","EZH2 Tyr646 gain-of-function mutation: 7.2% of follicular lymphoma, 21.7% of germinal-centre diffuse large B-cell lymphoma","CREBBP or EP300 inactivation: about 39% of diffuse large B-cell lymphoma, 41% of follicular lymphoma","TP53 mutation in mantle cell lymphoma: 11%, with median overall survival of 1.8 years against 12.7 years","RHOA G17V: 67 to 68% of angioimmunoblastic T-cell lymphoma, 18% of peripheral T-cell lymphoma not otherwise specified","9p24.1 alteration of the PD-1 ligand loci: 97% of 108 classical Hodgkin lymphomas","CIITA rearrangement: 38% of primary mediastinal B-cell lymphoma, 15% of classical Hodgkin lymphoma","t(11;18) API2-MALT1 in gastric MALT lymphoma: predicts failure of Helicobacter eradication","Immunoglobulin and T-cell receptor clonality: clonal, polyclonal or oligoclonal, read with the morphology and never alone","Deauville five-point score on interim and end-of-treatment PET","The immunophenotype, read by immunohistochemistry or flow cytometry (CD20, CD3, CD5, CD10, CD23, CD30, CD138, cyclin D1, ALK, BCL2, BCL6, MUM1), which assigns the entity and is the diagnosis","MYC, BCL2 and BCL6 rearrangements by fluorescence in situ hybridisation in every aggressive B-cell lymphoma, because MYC with BCL2 defines a separate entity","The Ki-67 proliferation index, which is above 95 per cent in Burkitt lymphoma and is part of the mantle cell risk score","Cell of origin in diffuse large B-cell lymphoma: germinal centre B-cell against activated B-cell","Epstein-Barr virus by EBER in situ hybridisation, which defines several entities and changes none of the treatment","Interim and end-of-treatment PET-CT, scored on the Deauville five-point scale","MYD88 L265P, which supports lymphoplasmacytic lymphoma and the immune-privileged large B-cell lymphomas","HTLV-1 serology where the person or their family comes from Japan, the Caribbean, west or central Africa, Iran, Romania or parts of South America"],"standardOfCare":[{"setting":"Aggressive B-cell (DLBCL and related)","approach":"Curative immunochemotherapy (R-CHOP or Pola-R-CHP); CAR-T or bispecific antibodies at relapse. See the DLBCL page.","refs":["rituximab","polatuzumab-vedotin"]},{"setting":"Indolent B-cell (follicular, marginal zone)","approach":"Watch and wait when asymptomatic; rituximab alone or with bendamustine or CHOP when treatment is needed; bispecifics and CAR-T for later relapses. See the follicular lymphoma page.","refs":["rituximab","bendamustine"]},{"setting":"Mantle cell lymphoma and CLL","approach":"BTK inhibitors and venetoclax-based regimens have largely replaced chemotherapy. See the mantle cell and CLL pages.","refs":["ibrutinib","venetoclax"]},{"setting":"T-cell lymphomas","approach":"CHOP-based chemotherapy, brentuximab vedotin for CD30-positive disease, transplant in first remission for fit patients. See the peripheral T-cell lymphoma page.","refs":["brentuximab-vedotin"]},{"setting":"How the treatment of a non-Hodgkin lymphoma is decided","approach":"Three questions, in order. Is it aggressive or indolent? Aggressive lymphomas (diffuse large B-cell, high-grade B-cell, Burkitt, most T-cell lymphomas, blastoid mantle cell) are treated immediately, with combination chemotherapy, with the intention to cure. Indolent lymphomas (follicular, marginal zone, lymphoplasmacytic) may not need treatment at all for years, and when they do the aim is control rather than cure. Is it a B-cell or a T-cell lymphoma? B-cell lymphomas carry CD20 and almost all first-line regimens contain an anti-CD20 antibody; T-cell lymphomas do not, which is the main reason their outcomes lag. Where is it, and what does it threaten? A lymphoma in the stomach, the brain, the testis, the eye or the skin is treated by rules specific to that site, not by the rules for nodal disease.\n\nThe things that must be done before the first dose are the same across the family: a proper biopsy reported to the current WHO classification, PET-CT staging reported by the Lugano classification, hepatitis B and HIV testing, and a fertility conversation.","refs":["lymphoma-type","lugano-classification","fdg-pet","lymphoma-tx-regimen-alphabet","lymphoma-tx-watch-and-wait","lymphoma-tx-hepatitis-b-reactivation","lymphoma-tx-fertility-preservation"],"guideline":{"version":"NCCN B-Cell and T-Cell Lymphomas; ESMO; WHO fifth edition; NCI PDQ","url":"https://www.cancer.gov/types/lymphoma/hp/adult-nhl-treatment-pdq"}},{"setting":"Supportive care that belongs to lymphoma specifically","approach":"Five things, each with its own entry. Tumour lysis syndrome: predictable from bulk, LDH and histology, prevented with fluids, allopurinol and, in high-risk patients, rasburicase; screen for glucose-6-phosphate dehydrogenase deficiency first. Hepatitis B reactivation: test surface antigen and core antibody before any anti-CD20 antibody and give entecavir or tenofovir prophylaxis, which in a randomised trial cut reactivation from 30 to 6.6 per cent against lamivudine. Pneumocystis and herpes prophylaxis with steroid-containing, purine-analogue, PI3K-inhibitor, CAR-T and bispecific regimens. Immunoglobulin replacement for those left with low IgG and recurrent infection after B-cell depletion. Cytokine release syndrome and ICANS after CAR-T and bispecific antibodies, graded by the ASTCT criteria and treated with tocilizumab and steroids. Fertility preservation before alkylating chemotherapy, arranged in days rather than weeks.","refs":["lymphoma-tx-tumour-lysis","lymphoma-tx-hepatitis-b-reactivation","lymphoma-tx-pjp-and-infection-prophylaxis","lymphoma-tx-immunoglobulin-replacement","lymphoma-tx-crs-icans","lymphoma-tx-fertility-preservation","rasburicase","tocilizumab","human-normal-immunoglobulin"],"guideline":{"version":"BSH guidelines; ASTCT consensus grading; NCCN supportive care","url":"https://doi.org/10.1016/j.bbmt.2018.12.758"}},{"setting":"Where British and American practice differ","approach":"In advanced Hodgkin lymphoma, the United States moved to nivolumab with AVD after SWOG S1826 while Germany moved to PET-guided BrECADD after HD21 and British practice sits between the two. In older mantle cell lymphoma, the British-led ENRICH trial made ibrutinib with rituximab a first-line option without chemotherapy, with the benefit concentrated against R-CHOP rather than against bendamustine-rituximab. In first-line diffuse large B-cell lymphoma, pola-R-CHP is the American default for IPI 2 and above while R-CHOP remains the commonest first treatment in England. Central nervous system prophylaxis has been dropped faster in the United Kingdom than in the United States. Access to bispecific antibodies and CAR-T exists in both countries by different routes: national commissioning and panel approval in England, insurance authorisation at an accredited centre in the United States.","refs":["lymphoma-tx-uk-versus-us","lymphoma-tx-uk-access","swog-s1826","hd21","polarix","triangle"],"guideline":{"version":"NICE; NCCN; ESMO; ENRICH, S1826, HD21","url":"https://doi.org/10.1016/S0140-6736(25)01432-1"}},{"setting":"Treatments that did not work, and are worth not being offered","approach":"DA-EPOCH-R as a general upgrade to R-CHOP failed in Alliance/CALGB 50303. Obinutuzumab in place of rituximab in diffuse large B-cell lymphoma failed in GOYA, although it works in follicular lymphoma in GALLIUM. Lenalidomide maintenance after R-CHOP lengthened progression-free survival but not life in REMARC. Tisagenlecleucel in second line failed in BELINDA while two other CAR-T products succeeded in the same setting. Four gray in two fractions is inferior to 24 gray for curative radiotherapy of indolent lymphoma in FoRT. Central nervous system prophylaxis did not lower central nervous system relapse below the rate predicted by CNS-IPI in the largest cohort that received it.","refs":["lymphoma-tx-failed-and-negative","belinda","gallium","lymphoma-tx-cns-prophylaxis","lymphoma-tx-maintenance","lymphoma-tx-radiotherapy"],"guideline":{"version":"The trials named","url":"https://doi.org/10.1200/JCO.18.01994"}}],"stateOfArt":["The antigens, and what they cost. Almost every surface target in lymphoma is a lineage antigen: a normal protein on a normal cell, present on the cancer because the cancer came from that cell. CD20 and CD19 are on every normal B cell, so the treatments that use them empty the B-cell compartment and leave low immunoglobulin and more infection behind; CD52 adds T cells and monocytes and produces the deepest lymphopenia of any antibody here; CCR4 is on regulatory T cells, which is why mogamulizumab causes rash and is associated with severe graft-versus-host disease if given shortly before an allogeneic transplant; CD47 is on red cells, so blocking it causes anaemia by design. CD30 is the exception, close to restricted to activated cells in an adult. CD3 is not on the tumour at all in B-cell disease: it is the handle a bispecific antibody uses to grip a T cell.","Which antigens can carry a payload. CD20 is not internalised, so it carries naked antibodies and T-cell engagers and no conjugate; CD79b, CD30 and CD22 are internalised, which is why the conjugates aim at them. This single property, not specificity, explains most of the format choices in lymphoma.","The B-cell receptor is the one pathway that picks a drug. Activated B-cell-like lymphoma signals continuously through CD79a and CD79b to SYK, BTK, PLC-gamma-2 and the CARD11-BCL10-MALT1 complex into NF-kB; the toll-like receptor arm feeds the same hub through MYD88 L265P. BTK inhibitors are standard in mantle cell lymphoma and Waldenstrom macroglobulinaemia and do little in germinal-centre disease.","The germinal centre explains the rest. To make a better antibody a B cell deliberately mutates its own DNA while dividing fast, with its damage response held down by BCL6 and its exit locked by polycomb. The translocations of BCL2 and MYC to an immunoglobulin locus are recombinase errors made during that programme, EZH2 gain-of-function mutations keep the exit locked, and CREBBP and EP300 loss leaves BCL6 active when it should be off.","Classification by molecule, honestly. Cell of origin is real, prognostic, and does not currently choose a treatment outside a trial. The genetic subtypes, MCD, BN2, N1, EZB and the rest, explain a great deal and change nothing today: no regulator licenses a drug on a LymphGen call and no randomised trial has assigned treatment by it. Two classifications apply only in practice: a MYC with BCL2 rearrangement, which moves most patients off R-CHOP, and an EZH2 mutation in relapsed follicular lymphoma, which opens tazemetostat.","Checkpoint blockade works in Hodgkin lymphoma for a genetic reason. The 9p24.1 amplicon carries both PD-1 ligand genes and JAK2, which induces them further, and 97% of 108 classical Hodgkin lymphomas carried concordant alterations of the two loci. PD-1 blockade gave an objective response in 20 of 23 heavily pre-treated patients; outside Hodgkin lymphoma and the mediastinal group, single-agent checkpoint blockade in B-cell lymphoma does very little.","Resistance, by class. Anti-CD20 is defeated by transcriptional loss of CD20, found in 5 of 19 rebiopsied relapses; covalent BTK inhibitors by BTK C481S, answered by a non-covalent inhibitor, and by PLCG2 gain of function, which no BTK inhibitor can reach; venetoclax by BCL2 G101V, which lowers drug affinity about 180-fold and appears months before progression; CD19 CAR-T by antigen loss, by the fitness of the collected T cells, and by the node the cells have to work in; and checkpoint blockade in Hodgkin lymphoma by loss of MHC class II rather than class I.","Tests, in practice. An excisional biopsy with an immunohistochemistry panel, FISH for MYC with BCL2 and BCL6, flow cytometry where cells can be put in suspension, immunoglobulin and T-cell receptor clonality where the morphology is equivocal, a gene panel where TP53, MYD88, EZH2 or a resistance mutation would change the plan, and FDG-PET scored on the Deauville five-point scale. Circulating tumour DNA can do all of genotyping, burden and residual disease, and no approval yet depends on it.","The B-cell side now has four ways of attacking the same cell surface and they stack: the naked antibody (rituximab, obinutuzumab), the antibody-drug conjugate (polatuzumab vedotin, brentuximab vedotin), the engineered T cell (CAR-T against CD19) and the bispecific antibody (glofitamab, epcoritamab, mosunetuzumab). A person whose large B-cell lymphoma relapses in 2026 has a realistic second and third chance of cure, which was not true in 2015.","The T-cell and NK-cell side has had one positive randomised first-line trial in twenty years, ECHELON-2, and it applies only to CD30-positive disease. Most of what is given in T-cell lymphoma is convention rather than demonstrated benefit, and the pages in this family say so where it is true.","The 2022 classifications moved several diseases from being a descriptive label to being a genetically defined entity: high-grade B-cell lymphoma with MYC and BCL2 rearrangements, the large B-cell lymphomas of immune-privileged sites, mediastinal grey zone lymphoma. Each of those moves exists because the genetics predicted the behaviour better than the appearance did.","PET-CT and the Deauville score made treatment adaptive. Scanning after two cycles and changing the plan on what the scan shows is now standard in Hodgkin lymphoma and is being tested across the aggressive B-cell lymphomas.","Infection remains the common cause of harm. Hepatitis B reactivation after anti-CD20 antibodies, Pneumocystis pneumonia on steroids, and low immunoglobulins for years after CAR-T or bispecific therapy each have a prevention that works and is sometimes forgotten."],"history":[{"year":1958,"title":"A jaw tumour in Ugandan children is described, and its geography points at a virus","note":"Burkitt's report in the British Journal of Surgery has no abstract indexed on Europe PMC; its importance is that mapping where the tumour occurred prompted the search for an infectious cause.","refs":["paper-burkitt-sarcoma-involving-jaws-african-children-br-j-surg-1958"]},{"year":1964,"title":"The first virus found in a human tumour","note":"Epstein, Achong and Barr saw virus particles in lymphoblasts cultured from one of Burkitt's biopsies, beginning the field that now includes human papillomavirus, hepatitis B and Helicobacter pylori.","refs":["paper-epstein-virus-particles-burkitt-lymphoblasts-lancet-1964"]},{"year":1971,"title":"Ann Arbor staging agreed","note":"A committee meeting in Ann Arbor, Michigan set out the four-stage anatomical system for Hodgkin's disease. Its descriptive language is still in use in 2026, inside the Lugano classification that replaced it.","refs":["lugano-classification"]},{"year":1980,"title":"The first human retrovirus, isolated from a T-cell lymphoma","note":"Poiesz and Gallo characterised type C particles with a reverse transcriptase unlike any known primate retrovirus; Hinuma's Japanese seroepidemiology the following year found antibodies in all 44 patients with adult T-cell leukaemia tested and in 26 per cent of healthy adults from endemic areas.","refs":["paper-poiesz-htlv-retrovirus-cutaneous-t-cell-lymphoma-pnas-1980","paper-hinuma-adult-t-cell-leukaemia-antigen-pnas-1981"]},{"year":1982,"title":"MYC is mapped to the Burkitt translocation","note":"The human c-myc gene is placed at 8q24, the region translocated to chromosome 2, 14 or 22 in Burkitt lymphoma cells, tying an oncogene to a specific chromosome swap for the first time in a human cancer.","refs":["myc-gene","double-hit-rearrangement"]},{"year":1985,"title":"t(14;18) is shown to be a recombinase error","note":"The breakpoint sequences carry N-region nucleotides and lie beside signal-like sequences, which places the founding lesion of follicular lymphoma at the pre-B-cell stage, years before the disease.","refs":["bcl2","bcl2-rearrangement"]},{"year":1993,"title":"The International Prognostic Index","note":"Built from 2,031 patients with aggressive lymphoma treated at 16 institutions across the United States, Europe and Canada. It counts age, stage, lactate dehydrogenase, performance status and extranodal sites, and it still decides treatment intensity in 2026.","refs":["ipi-score"]},{"year":1994,"title":"The Reed-Sternberg cell is proved to be a clonal B cell","note":"Single cells picked off a histological section with a micromanipulator each gave one clonal immunoglobulin rearrangement, settling the identity of a cell that had lost almost every B-cell marker.","refs":["lymphoma-bio-hodgkin-microenvironment"]},{"year":1997,"title":"Rituximab approved, the first antibody for a cancer","note":"Anti-CD20 rituximab for relapsed follicular lymphoma; added to CHOP it raised cure rates in diffuse large B-cell lymphoma.","refs":["rituximab"]},{"year":2000,"title":"Cell of origin","note":"Microarray profiling splits diffuse large B-cell lymphoma into germinal-centre B-cell-like and activated B-cell-like forms with different survival, the first molecular classification of a lymphoma.","refs":["cell-of-origin","lymphoma-bio-cell-of-origin-in-practice"]},{"year":2002,"title":"Gene expression turns one lymphoma into three","note":"Rosenwald profiled 240 biopsies, found germinal-centre, activated and type 3 subgroups and built a 17-gene survival predictor independent of the International Prognostic Index; Hans reproduced the split in 2004 with three ordinary stains, giving five-year survival of 76 against 34 per cent.","refs":["paper-rosenwald-molecular-profiling-dlbcl-nejm-2002","paper-hans-immunohistochemistry-cell-of-origin-dlbcl-blood-2004","paper-alizadeh-nature"]},{"year":2003,"title":"Clonality testing is standardised","note":"The BIOMED-2 collaboration reduces immunoglobulin and T-cell receptor clonality to 107 primers in 18 tubes, making the result comparable between laboratories.","refs":["clonality-testing","ig-tcr-clonality"]},{"year":2004,"title":"Cell of origin becomes three stains","note":"The Hans algorithm reproduces the microarray split with CD10, BCL6 and MUM1 on a tissue microarray, with five-year survival of 76% against 34%, which is why most laboratories report non-germinal-centre rather than activated.","refs":["cell-of-origin"]},{"year":2007,"title":"The only randomised trial ever run in adult T-cell leukaemia/lymphoma","note":"JCOG9801, 118 patients: complete response 40 against 25 per cent for VCAP-AMP-VECP over biweekly CHOP, three-year overall survival 24 against 13 per cent, grade 4 thrombocytopenia 74 against 17 per cent.","refs":["paper-jcog9801-vcap-amp-vecp-adult-t-cell-leukaemia-jco-2007","jcog9801"]},{"year":2010,"title":"Chronic active B-cell receptor signalling, and the 9p24.1 amplicon","note":"Two findings in one year: activated B-cell-like lymphoma depends on continuous B-cell receptor signalling through BTK, which is the rationale for every BTK inhibitor; and Hodgkin lymphoma and mediastinal large B-cell lymphoma amplify the locus carrying both PD-1 ligands and JAK2, which is the rationale for checkpoint blockade there.","refs":["btk","cd79b","jak2","pd-ligand-9p24-alteration"]},{"year":2010,"title":"EZH2 Tyr641 mutations","note":"Gain-of-function substitutions at a single tyrosine in the SET domain are found in 21.7% of germinal-centre large B-cell lymphomas and 7.2% of follicular lymphomas, and absent from the activated subtype; tazemetostat follows.","refs":["ezh2","ezh2-y646-mutation"]},{"year":2011,"title":"MYD88 L265P, and the chromatin genes","note":"An oncogenic MYD88 substitution is found in 29% of activated B-cell-like lymphomas; in the same period CREBBP and EP300 inactivation is found in about 39% of diffuse large B-cell and 41% of follicular lymphoma, and KMT2D in 32% and 89%, which makes lymphoma a disease of chromatin and not only of signalling.","refs":["myd88","crebbp","kmt2d","myd88-l265p"]},{"year":2011,"title":"Asparaginase makes NK/T-cell lymphoma treatable, and rituximab maintenance doubles remission in follicular lymphoma","note":"SMILE reached an overall response of 79 per cent in 38 patients with a disease that resists anthracyclines; PRIMA raised three-year progression-free survival from 57.6 to 74.9 per cent, and at nine years the medians were 10.5 against 4.1 years with no survival difference.","refs":["paper-smile-chemotherapy-nk-t-cell-lymphoma-jco-2011","paper-prima-rituximab-maintenance-follicular-lancet-2011","paper-prima-final-rituximab-maintenance-follicular-jco-2019","smile-enktl","prima-follicular"]},{"year":2012,"title":"MYD88 L265P defines Waldenstrom macroglobulinaemia","note":"Whole-genome sequencing finds the same substitution in all 10 paired cases and in 91% of lymphoplasmacytic lymphoma overall, absent from normal tissue, which turns a diagnosis of exclusion into a genotype.","refs":["myd88","myd88-l265p"]},{"year":2014,"title":"Resistance to a BTK inhibitor is read in the kinase","note":"BTK C481S in five of six patients with acquired ibrutinib resistance and PLCG2 gain-of-function mutations in two, which is why the non-covalent inhibitors exist.","refs":["btk","plcg2","btk-c481s"]},{"year":2014,"title":"RHOA G17V in angioimmunoblastic T-cell lymphoma","note":"A single substitution in 67 to 68% of cases, specific to the tumour cells, with the accompanying TET2 mutations also present in normal blood cells, which places this lymphoma as a growth out of clonal haematopoiesis.","refs":["rhoa","tet2","rhoa-g17v"]},{"year":2014,"title":"The Lugano classification","note":"Agreed at the International Conference on Malignant Lymphoma, it made PET-CT the standard staging test for lymphomas that take up the tracer, restricted the A and B symptom suffixes to Hodgkin lymphoma, and removed routine bone marrow biopsy from the staging of Hodgkin lymphoma.","refs":["lugano-classification","fdg-pet","deauville-score"]},{"year":2015,"title":"Antigen escape after CAR-T is explained","note":"Relapse without CD19 turns out to combine deletion, exon 2 mutation and selection for an alternatively spliced transcript that skips the epitope and still partly works, which is why a standard sequencing test can call the gene normal.","refs":["cd19","lymphoma-bio-antigen-escape"]},{"year":2015,"title":"Checkpoint blockade in Hodgkin lymphoma","note":"Nivolumab produces an objective response in 20 of 23 heavily pre-treated patients, most of whom had already failed autologous transplant and brentuximab vedotin.","refs":["pd-ligand-9p24-alteration","nivolumab"]},{"year":2015,"title":"Early progression splits follicular lymphoma in two","note":"Casulo: 19 per cent of 588 patients progressed within two years of first-line R-CHOP, with five-year overall survival of 50 against 90 per cent and an index-adjusted hazard ratio of 6.44.","refs":["paper-casulo-pod24-follicular-lymphoma-jco-2015","lymphoma-tx-pod24"]},{"year":2016,"title":"A blood test reads the lymphoma without a biopsy","note":"Scherer showed circulating tumour DNA predicts outcome at diagnosis, classifies cell of origin from plasma, beats imaging for residual disease and distinguishes follicular lymphomas that will transform from those that will not.","refs":["paper-scherer-ctdna-lymphoma-subtypes-genome-evolution-sci-transl-med-2016","paper-kurtz-j-clin-oncol","ctdna"]},{"year":2017,"title":"First CAR-T for lymphoma","note":"Axicabtagene ciloleucel approved for relapsed large B-cell lymphoma after two or more lines.","refs":["axicabtagene-ciloleucel"]},{"year":2018,"title":"The genetic subtypes","note":"Two large series read large B-cell lymphoma as four and five genetically defined groups, MCD, BN2, N1 and EZB among them, with different outcomes after immunochemotherapy.","refs":["lymphoma-bio-lymphgen"]},{"year":2018,"title":"Two genetic classifications of diffuse large B-cell lymphoma, three weeks apart","note":"Chapuy's five clusters from 304 tumours and Schmitz's four subtypes from 574; Wright's LymphGen tool in 2020 extended them to seven and made per-patient classification possible. None has yet changed a first-line treatment.","refs":["paper-chapuy-molecular-subtypes-dlbcl-nat-med-2018","paper-schmitz-genetics-pathogenesis-dlbcl-nejm-2018","paper-wright-lymphgen-genetic-subtypes-dlbcl-cancer-cell-2020","lymphoma-ev-genetic-subtype-directed-first-line"]},{"year":2019,"title":"Venetoclax resistance is a single amino acid","note":"BCL2 G101V, found at progression in 7 of 15 paired patients and in none at study entry, lowers drug affinity about 180-fold and is detectable months before clinical relapse.","refs":["bcl2","bcl2-g101v"]},{"year":2019,"title":"Four cycles instead of six, and a targeted tablet that helped the young and harmed the old","note":"FLYER: three-year progression-free survival 96 per cent with four cycles of R-CHOP in young favourable disease, non-inferior to six. PHOENIX: ibrutinib improved event-free survival under 60 (hazard ratio 0.579) and worsened it over 60, raising serious adverse events from 38.2 to 63.4 per cent.","refs":["paper-flyer-four-vs-six-cycles-r-chop-lancet-2019","paper-phoenix-ibrutinib-r-chop-non-gcb-dlbcl-jco-2019","flyer"]},{"year":2020,"title":"LymphGen makes the genetic subtypes usable on one patient","note":"A probabilistic classifier assigns a lymphoma to one of seven genetic subtypes and shows each shares a pathogenesis with a particular indolent or extranodal lymphoma. No randomised trial has yet assigned treatment by it.","refs":["lymphoma-bio-lymphgen"]},{"year":2020,"title":"The third CAR-T product, and the mantle cell question changes shape","note":"TRANSCEND NHL 001: objective response 73 per cent and complete response 53 per cent in 256 evaluable patients, with grade 3 or worse cytokine release syndrome in 2 per cent. SHINE then gained 28 months of progression-free survival in older mantle cell lymphoma with no survival benefit.","refs":["paper-transcend-nhl-001-liso-cel-lancet-2020","paper-shine-ibrutinib-bendamustine-rituximab-mantle-cell-nejm-2022","transcend-nhl-001","shine"]},{"year":2021,"title":"Residual disease at parts per million","note":"PhasED-seq uses several mutations carried on one DNA fragment, which lymphoma genomes supply because of somatic hypermutation, and finds residual disease in a further 25% of participants called negative by the previous method.","refs":["ctdna-lymphoma-monitoring","ctdna-mrd-positive"]},{"year":2022,"title":"The WHO fifth edition","note":"High-grade B-cell lymphoma with MYC and BCL2 rearrangements becomes an entity of its own and the T-follicular-helper lymphomas are grouped by origin rather than appearance. A second classification published the same year disagrees on several names.","refs":["double-hit-rearrangement"]},{"year":2022,"title":"Two classifications instead of one","note":"The fifth edition of the WHO classification and the International Consensus Classification were published within months of each other. They agree about most entities and differ about several names and boundaries, which is why a report may give a disease a name that a trial protocol does not recognise.","refs":["lymphoma-classification-2022"]},{"year":2022,"title":"The second-line CAR-T trial that failed, and why","note":"BELINDA: median event-free survival 3.0 months in both arms, with a 52-day median interval from leukapheresis to infusion and 25.9 per cent of the CAR-T group progressing by week 6 against 13.8 per cent of the comparator group.","refs":["paper-belinda-tisagenlecleucel-second-line-nejm-2022","belinda","lymphoma-ev-manufacturing-time-as-a-trial-endpoint"]},{"year":2023,"title":"Bispecific antibodies approved","note":"Glofitamab and epcoritamab, off-the-shelf CD20 x CD3 antibodies, approved for relapsed large B-cell lymphoma.","refs":["glofitamab","epcoritamab"]},{"year":2025,"title":"A chemotherapy-free first line beats immunochemotherapy in mantle cell lymphoma","note":"ENRICH, 397 patients: adjusted progression-free survival hazard ratio 0.69, driven by the comparison against R-CHOP (0.37) rather than against bendamustine-rituximab (0.91). ECHELON-3 and POLARGO gave transplant-ineligible relapsed diffuse large B-cell lymphoma two more options with a survival benefit.","refs":["paper-enrich-ibrutinib-rituximab-mantle-cell-lancet-2025","paper-echelon-3-brentuximab-lenalidomide-rituximab-dlbcl-jco-2025","paper-polargo-polatuzumab-r-gemox-dlbcl-jco-2026","enrich","polargo"]},{"year":2032,"title":"The first-line bispecific question completes","note":"The National Cancer Institute trial of mosunetuzumab against rituximab in low tumour burden follicular lymphoma (NCT06337318, 600 estimated participants) has a primary completion date of 31 March 2032; RADAR, the radiotherapy-free Hodgkin trial, is listed for September 2030.","refs":["mosun-lbt-fl","radar-hodgkin","lymphoma-ev-fixed-duration-chemotherapy-free-first-line"]}],"pipeline":["glofitamab","epcoritamab","mosunetuzumab","obecabtagene-autoleucel","tqb3702","stp938","lymphoma-ev-genetic-subtype-directed-first-line","lymphoma-ev-ctdna-instead-of-the-interim-scan","lymphoma-ev-radiotherapy-free-early-hodgkin","lymphoma-ev-fixed-duration-chemotherapy-free-first-line","lymphoma-ev-randomised-evidence-for-the-t-cell-lymphomas","lymphoma-ev-manufacturing-time-as-a-trial-endpoint","lymphoma-ev-the-drugs-that-cure-and-the-places-without-them","lymphoma-ev-late-effects-of-the-treatments-given-now"],"openProblems":["Relapsed T-cell lymphomas still lack effective options.","Access to CAR-T and bispecifics outside high-income countries.","The genetic classifications of large B-cell lymphoma are the best-validated molecular taxonomy in haematology and no randomised trial has yet assigned treatment by one. Patients are genotyped, told which subtype they have, and then given the same regimen as everyone else.","Cell of origin has been known for a quarter of a century and every randomised attempt to act on it in first line has failed to change survival in the whole population. It is not clear whether the problem is the classification, the drugs chosen, or the fact that immunohistochemistry cannot separate the activated type from the unclassified one.","Nobody knows how often a large B-cell lymphoma relapses without CD19 after CAR-T. The published series are small and do not agree, and most relapses are not rebiopsied at all, so the field is choosing second treatments without the measurement that would decide between them.","The same is true of CD20: the only series that looked found 5 of 19 rebiopsied relapses had lost the antigen, which means the denominator for every other patient is unknown and a second anti-CD20 drug is often given without checking the target is still there.","MYC has been a known driver of Burkitt lymphoma since 1982 and there is still no drug that acts on it. The regimens that cure Burkitt lymphoma are the most toxic in lymphoma, which is why it remains hardest to treat in older patients and in the equatorial regions where the endemic form occurs.","Circulating tumour DNA in lymphoma can genotype, measure burden and find residual disease at parts per million, and no trial has yet shown that changing treatment on the result helps anyone.","BCL2 was the first apoptosis gene found in a human cancer and venetoclax has not repeated its chronic lymphocytic leukaemia result in follicular or large B-cell lymphoma, because those cells also lean on MCL1 and BCL-xL. MCL1 inhibitors have been held back by cardiac toxicity.","The T-cell and NK-cell lymphomas are about one lymphoma in twenty and have a small fraction of the trials, the drugs and the survival gains of the B-cell lymphomas. Five-year relative survival in the UK population series was 45.4 per cent across T-cell lymphomas against 68.8 per cent across B-cell lymphomas.","Several of these diseases are common where trials are not run. Extranodal NK/T-cell lymphoma is a disease of east Asia and Latin America; adult T-cell leukaemia/lymphoma is a disease of south-western Japan, the Caribbean and west Africa. The treatments with the best evidence were developed there, and are least available to people from those populations living elsewhere.","Two reference classifications were published in 2022 and they disagree about names and boundaries. A patient can be told they have three different diagnoses depending on which book the pathologist used and which trial they are being screened for.","CAR-T and bispecific antibodies are available in a small number of countries and in a small number of centres within them. The gap between what is possible and what is reachable is now the main determinant of outcome in relapsed large B-cell lymphoma.","There is no way to predict which indolent lymphoma will transform into an aggressive one, and transformation is the commonest cause of death in follicular lymphoma.","Three genetic classifications of diffuse large B-cell lymphoma exist and none of them decides anyone's first-line treatment outside a trial. The gap between Schmitz in 2018 and a randomised trial that assigns treatment by LymphGen subtype is the clearest unfinished business in the disease.","Circulating tumour DNA predicts outcome at diagnosis, detects residual disease better than imaging and flags transformation before it declares itself, and no randomised trial has yet shown that changing treatment on the strength of it helps anyone.","The T-cell lymphomas have almost no randomised evidence. Adult T-cell leukaemia/lymphoma has had exactly one controlled trial, opened in 1998 with 118 patients, and the regimen that makes extranodal NK/T-cell lymphoma treatable rests on a 38-patient single-arm study.","Rituximab is thirty years old and still unavailable or unaffordable in much of the world, asparaginase is subject to recurrent shortages, and CAR-T needs an apheresis service and a cryopreservation chain. Lymphoma is among the most curable common cancers in the places that have the drugs."],"basics":{"symptoms":["A painless, persistent swelling of a lymph node in the neck, armpit or groin, usually over weeks rather than days, that does not go down after an infection clears.","The B symptoms: drenching night sweats that soak nightclothes, unexplained fever, and weight loss of more than a tenth of body weight in six months. They are recorded formally in the stage for Hodgkin lymphoma and noted but not staged in non-Hodgkin lymphoma.","Itching without a rash, fatigue out of proportion to activity, and loss of appetite.","Symptoms of the organ involved where the lymphoma is extranodal: indigestion and anaemia in gastric lymphoma, a painless lump in the testis, a bulging or displaced eye, a skin patch that has been treated as eczema for years, abdominal pain or perforation in intestinal lymphoma, headache or confusion in lymphoma of the central nervous system.","Swelling of the face and arms with breathlessness, which is superior vena cava obstruction from a large chest mass, and is an emergency: it is the usual presentation of primary mediastinal B-cell lymphoma and of mediastinal grey zone lymphoma."],"diagnosis":["An excision biopsy of a whole lymph node where that is possible, because the architecture of the node is part of the diagnosis and a needle core may not show it. A fine-needle aspirate is not sufficient to diagnose lymphoma.","Immunohistochemistry and flow cytometry on the biopsy, which identify the lineage and the entity, followed by fluorescence in situ hybridisation for the rearrangements that define separate diseases.","Blood tests: full blood count, lactate dehydrogenase, kidney and liver function, calcium, and virology for hepatitis B, hepatitis C and HIV before any antibody treatment, because anti-CD20 antibodies can reactivate hepatitis B.","PET-CT from the skull base to mid-thigh for the lymphomas that take up the tracer; CT alone for those that do not.","A bone marrow biopsy where it will change the stage or the treatment. The Lugano classification removed it from routine staging of Hodgkin lymphoma and from most diffuse large B-cell lymphoma staged by PET.","A lumbar puncture, an MRI of the brain, or an eye examination where the subtype or the sites involved carry a risk to the central nervous system."],"staging":["The Lugano classification (2014), which modified the Ann Arbor system of 1971: stage I, one lymph node region; stage II, two or more on the same side of the diaphragm; stage III, both sides; stage IV, diffuse involvement of an organ outside the lymphatic system.","The suffix E marks a single extranodal site reached by direct extension, and the suffixes A and B for the absence or presence of fever, night sweats and weight loss are formally recorded only for Hodgkin lymphoma.","Bulk is recorded separately: a single mass of 10 cm or more, or more than a third of the width of the chest, which changes treatment in several subtypes.","Stage matters less in lymphoma than in solid cancers. The prognosis is read from a score: the International Prognostic Index for aggressive lymphoma, FLIPI for follicular, MIPI for mantle cell and the Prognostic Index for T-cell lymphoma for the nodal T-cell lymphomas.","Stage IV lymphoma is routinely treated with the intention to cure, which is not what stage IV means in most other cancers."],"sources":[{"label":"Lugano classification: recommendations for initial evaluation, staging and response assessment of Hodgkin and non-Hodgkin lymphoma (Cheson, J Clin Oncol 2014)","url":"https://doi.org/10.1200/JCO.2013.54.8800"},{"label":"Report of the Committee on Hodgkin's Disease Staging Classification (Carbone, Cancer Research 1971, 31:1860 to 1861)","url":"https://pubmed.ncbi.nlm.nih.gov/5121694/"},{"label":"A predictive model for aggressive non-Hodgkin's lymphoma: the International Prognostic Index (N Engl J Med 1993)","url":"https://doi.org/10.1056/NEJM199309303291402"},{"label":"Peripheral T-cell lymphoma unspecified: the Prognostic Index for T-cell lymphoma (Gallamini, Blood 2004)","url":"https://doi.org/10.1182/blood-2003-09-3080"},{"label":"NCI PDQ: adult non-Hodgkin lymphoma treatment (health professional version)","url":"https://www.cancer.gov/types/lymphoma/hp/adult-nhl-treatment-pdq"},{"label":"Lymphoma Action: types of lymphoma (UK patient charity)","url":"https://lymphoma-action.org.uk/types-lymphoma"}]},"prognosis":{"text":"The figures for non-Hodgkin lymphoma as a whole are the average of more than sixty diseases and apply exactly to nobody, which is the reason to read the subtype page instead. With that said: in the United Kingdom, 64.6 per cent of people diagnosed with non-Hodgkin lymphoma are alive ten years later (Cancer Research UK), and in the United States five-year relative survival was 74.3 per cent for 2016 to 2022, up from about 47 per cent in the mid-1970s (SEER). The spread behind those averages is very wide. In the UK population series that reports survival by subtype, five-year relative survival ran from 86.5 per cent in follicular lymphoma and 87.9 per cent in extranodal marginal zone lymphoma, through 54.8 per cent in diffuse large B-cell lymphoma, to 31.4 per cent in mantle cell lymphoma and 45.4 per cent across the T-cell lymphomas as a group; those figures are for people diagnosed between 2004 and 2012 and followed to 2014, so they predate the bispecific antibodies, CAR-T and the newer mantle cell regimens, and they understate what is achieved today in several subtypes.","sources":[{"label":"Cancer Research UK: non-Hodgkin lymphoma statistics (incidence, mortality, survival)","url":"https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/non-hodgkin-lymphoma"},{"label":"SEER Cancer Stat Facts: non-Hodgkin lymphoma (United States incidence, mortality and relative survival)","url":"https://seer.cancer.gov/statfacts/html/nhl.html"},{"label":"Lymphoma incidence, survival and prevalence 2004 to 2014, subtype analyses from the UK Haematological Malignancy Research Network (Smith, Br J Cancer 2015)","url":"https://doi.org/10.1038/bjc.2015.94"}]}},"route":"/cancers/non-hodgkin-lymphoma/","neighbours":{"cancer":[{"id":"adult-t-cell-leukaemia-lymphoma","kind":"cancer","name":"Adult T-cell leukaemia/lymphoma","route":"/cancers/adult-t-cell-leukaemia-lymphoma/"},{"id":"alk-negative-anaplastic-large-cell-lymphoma","kind":"cancer","name":"ALK-negative anaplastic large cell lymphoma","route":"/cancers/alk-negative-anaplastic-large-cell-lymphoma/"},{"id":"alk-positive-anaplastic-large-cell-lymphoma","kind":"cancer","name":"ALK-positive anaplastic large cell lymphoma","route":"/cancers/alk-positive-anaplastic-large-cell-lymphoma/"},{"id":"breast-implant-associated-alcl","kind":"cancer","name":"Breast implant-associated anaplastic large cell lymphoma","route":"/cancers/breast-implant-associated-alcl/"},{"id":"burkitt-lymphoma","kind":"cancer","name":"Burkitt lymphoma","route":"/cancers/burkitt-lymphoma/"},{"id":"cll","kind":"cancer","name":"Chronic lymphocytic leukaemia","route":"/cancers/cll/"},{"id":"dlbcl","kind":"cancer","name":"Diffuse large B-cell lymphoma","route":"/cancers/dlbcl/"},{"id":"ebv-positive-dlbcl","kind":"cancer","name":"EBV-positive diffuse large B-cell lymphoma","route":"/cancers/ebv-positive-dlbcl/"},{"id":"enteropathy-associated-t-cell-lymphoma","kind":"cancer","name":"Enteropathy-associated T-cell lymphoma","route":"/cancers/enteropathy-associated-t-cell-lymphoma/"},{"id":"extranodal-nk-t-cell-lymphoma","kind":"cancer","name":"Extranodal NK/T-cell lymphoma","route":"/cancers/extranodal-nk-t-cell-lymphoma/"},{"id":"follicular-lymphoma","kind":"cancer","name":"Follicular lymphoma","route":"/cancers/follicular-lymphoma/"},{"id":"gastric-malt-lymphoma","kind":"cancer","name":"Gastric MALT lymphoma","route":"/cancers/gastric-malt-lymphoma/"},{"id":"high-grade-b-cell-lymphoma-myc-bcl2","kind":"cancer","name":"High-grade B-cell lymphoma with MYC and BCL2 rearrangements (double-hit lymphoma)","route":"/cancers/high-grade-b-cell-lymphoma-myc-bcl2/"},{"id":"hiv-associated-lymphoma","kind":"cancer","name":"HIV-associated (AIDS-related) lymphomas","route":"/cancers/hiv-associated-lymphoma/"},{"id":"hodgkin-lymphoma","kind":"cancer","name":"Hodgkin lymphoma","route":"/cancers/hodgkin-lymphoma/"},{"id":"lymphomatoid-granulomatosis","kind":"cancer","name":"Lymphomatoid granulomatosis","route":"/cancers/lymphomatoid-granulomatosis/"},{"id":"mantle-cell-lymphoma","kind":"cancer","name":"Mantle cell lymphoma","route":"/cancers/mantle-cell-lymphoma/"},{"id":"marginal-zone-lymphoma","kind":"cancer","name":"Marginal zone lymphoma","route":"/cancers/marginal-zone-lymphoma/"},{"id":"mediastinal-grey-zone-lymphoma","kind":"cancer","name":"Mediastinal grey zone lymphoma","route":"/cancers/mediastinal-grey-zone-lymphoma/"},{"id":"monomorphic-epitheliotropic-intestinal-t-cell-lymphoma","kind":"cancer","name":"Monomorphic epitheliotropic intestinal T-cell lymphoma","route":"/cancers/monomorphic-epitheliotropic-intestinal-t-cell-lymphoma/"},{"id":"mycosis-fungoides","kind":"cancer","name":"Mycosis fungoides","route":"/cancers/mycosis-fungoides/"},{"id":"ocular-adnexal-malt-lymphoma","kind":"cancer","name":"Ocular adnexal MALT lymphoma","route":"/cancers/ocular-adnexal-malt-lymphoma/"},{"id":"peripheral-t-cell-lymphoma","kind":"cancer","name":"Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma)","route":"/cancers/peripheral-t-cell-lymphoma/"},{"id":"plasmablastic-lymphoma","kind":"cancer","name":"Plasmablastic lymphoma","route":"/cancers/plasmablastic-lymphoma/"},{"id":"post-transplant-lymphoproliferative-disorder","kind":"cancer","name":"Post-transplant lymphoproliferative disorder (PTLD)","route":"/cancers/post-transplant-lymphoproliferative-disorder/"},{"id":"primary-cns-lymphoma","kind":"cancer","name":"Primary CNS lymphoma","route":"/cancers/primary-cns-lymphoma/"},{"id":"primary-effusion-lymphoma","kind":"cancer","name":"Primary effusion lymphoma","route":"/cancers/primary-effusion-lymphoma/"},{"id":"primary-testicular-lymphoma","kind":"cancer","name":"Primary large B-cell lymphoma of the testis","route":"/cancers/primary-testicular-lymphoma/"},{"id":"primary-mediastinal-b-cell-lymphoma","kind":"cancer","name":"Primary mediastinal (thymic) large B-cell lymphoma","route":"/cancers/primary-mediastinal-b-cell-lymphoma/"},{"id":"t-cell-histiocyte-rich-large-b-cell-lymphoma","kind":"cancer","name":"T-cell/histiocyte-rich large B-cell lymphoma","route":"/cancers/t-cell-histiocyte-rich-large-b-cell-lymphoma/"},{"id":"waldenstrom","kind":"cancer","name":"Waldenström macroglobulinaemia","route":"/cancers/waldenstrom/"}],"biomarker":[{"id":"pd-ligand-9p24-alteration","kind":"biomarker","name":"9p24.1 alteration of the PD-1 ligand loci","route":"/biomarkers/pd-ligand-9p24-alteration/"},{"id":"bcl2-g101v","kind":"biomarker","name":"BCL2 G101V and the other venetoclax binding-site mutations","route":"/biomarkers/bcl2-g101v/"},{"id":"bcl2-rearrangement","kind":"biomarker","name":"BCL2 rearrangement, t(14;18)","route":"/biomarkers/bcl2-rearrangement/"},{"id":"btk-c481s","kind":"biomarker","name":"BTK resistance mutations: C481S, and L528W and T474I after the non-covalent inhibitors","route":"/biomarkers/btk-c481s/"},{"id":"cd19-expression","kind":"biomarker","name":"CD19 expression (CD19-positive)","route":"/biomarkers/cd19-expression/"},{"id":"cd20-expression","kind":"biomarker","name":"CD20 expression (CD20-positive)","route":"/biomarkers/cd20-expression/"},{"id":"cd22-expression","kind":"biomarker","name":"CD22 expression (CD22-positive)","route":"/biomarkers/cd22-expression/"},{"id":"cd30-expression","kind":"biomarker","name":"CD30 expression (CD30-positive)","route":"/biomarkers/cd30-expression/"},{"id":"cd38-expression","kind":"biomarker","name":"CD38 expression","route":"/biomarkers/cd38-expression/"},{"id":"cd79b-itam-mutation","kind":"biomarker","name":"CD79B ITAM mutation","route":"/biomarkers/cd79b-itam-mutation/"},{"id":"ctdna-mrd-positive","kind":"biomarker","name":"ctDNA MRD positivity (molecular residual disease after curative treatment)","route":"/biomarkers/ctdna-mrd-positive/"},{"id":"myc-bcl2-double-expressor","kind":"biomarker","name":"Double expressor: MYC and BCL2 protein together by immunohistochemistry","route":"/biomarkers/myc-bcl2-double-expressor/"},{"id":"double-hit-rearrangement","kind":"biomarker","name":"Double-hit and triple-hit: MYC with BCL2 and BCL6 rearrangement","route":"/biomarkers/double-hit-rearrangement/"},{"id":"ezh2-y646-mutation","kind":"biomarker","name":"EZH2 gain-of-function mutation (Tyr646, originally Tyr641)","route":"/biomarkers/ezh2-y646-mutation/"},{"id":"ig-tcr-clonality","kind":"biomarker","name":"Immunoglobulin and T-cell receptor clonality","route":"/biomarkers/ig-tcr-clonality/"},{"id":"rhoa-g17v","kind":"biomarker","name":"RHOA G17V","route":"/biomarkers/rhoa-g17v/"},{"id":"tp53-del17p","kind":"biomarker","name":"TP53 mutation and del(17p)","route":"/biomarkers/tp53-del17p/"}],"roadmap":[{"id":"lymphoma-roadmap","kind":"roadmap","name":"Lymphoma roadmap: from a jaw tumour in Uganda and the first human cancer virus to gene-expression subtypes, PET-adapted chemotherapy, CAR-T cells, bispecific antibodies and the genetics-directed trials now recruiting","route":"/roadmaps/lymphoma-roadmap/"}],"idea":[{"id":"lymphoma-ev-radiotherapy-free-early-hodgkin","kind":"idea","name":"A radiotherapy-free cure for early Hodgkin lymphoma that actually holds","route":"/ideas/lymphoma-ev-radiotherapy-free-early-hodgkin/"},{"id":"lymphoma-ev-genetic-subtype-directed-first-line","kind":"idea","name":"Assign first-line treatment in diffuse large B-cell lymphoma by genetic subtype, not by a three-antibody stain","route":"/ideas/lymphoma-ev-genetic-subtype-directed-first-line/"},{"id":"lymphoma-ev-fixed-duration-chemotherapy-free-first-line","kind":"idea","name":"Fixed-duration, chemotherapy-free first-line treatment for the indolent lymphomas","route":"/ideas/lymphoma-ev-fixed-duration-chemotherapy-free-first-line/"},{"id":"lymphoma-ev-late-effects-of-the-treatments-given-now","kind":"idea","name":"Measure the late effects of the treatments being given now, not the ones given in 1975","route":"/ideas/lymphoma-ev-late-effects-of-the-treatments-given-now/"},{"id":"lymphoma-ev-randomised-evidence-for-the-t-cell-lymphomas","kind":"idea","name":"Randomised evidence for the T-cell lymphomas, including the ones that are not in Europe or North America","route":"/ideas/lymphoma-ev-randomised-evidence-for-the-t-cell-lymphomas/"},{"id":"lymphoma-ev-manufacturing-time-as-a-trial-endpoint","kind":"idea","name":"Report the time from apheresis to infusion as a trial endpoint, not a logistics footnote","route":"/ideas/lymphoma-ev-manufacturing-time-as-a-trial-endpoint/"},{"id":"lymphoma-ev-the-drugs-that-cure-and-the-places-without-them","kind":"idea","name":"The drugs that cure lymphoma, and the places that do not have them","route":"/ideas/lymphoma-ev-the-drugs-that-cure-and-the-places-without-them/"},{"id":"lymphoma-ev-ctdna-instead-of-the-interim-scan","kind":"idea","name":"Use circulating tumour DNA instead of the interim scan to decide what happens next","route":"/ideas/lymphoma-ev-ctdna-instead-of-the-interim-scan/"}],"technology":[{"id":"adc","kind":"technology","name":"Antibody-drug conjugate (ADC)","route":"/technologies/adc/"},{"id":"autologous-stem-cell-transplant","kind":"technology","name":"Autologous stem cell transplant (high-dose therapy)","route":"/technologies/autologous-stem-cell-transplant/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"},{"id":"capsule-endoscopy-systems","kind":"technology","name":"Capsule endoscopy (PillCam, EndoCapsule, CapsoCam)","route":"/technologies/capsule-endoscopy-systems/"},{"id":"car-t","kind":"technology","name":"CAR-T cell therapy","route":"/technologies/car-t/"},{"id":"closed-system-transfer-devices","kind":"technology","name":"Closed-system transfer devices for hazardous drugs (PhaSeal, ChemoLock, Equashield)","route":"/technologies/closed-system-transfer-devices/"},{"id":"cbt-fatigue-distress","kind":"technology","name":"Cognitive behavioural therapy for fatigue and distress","route":"/technologies/cbt-fatigue-distress/"},{"id":"cgp","kind":"technology","name":"Comprehensive genomic profiling","route":"/technologies/cgp/"},{"id":"ctdna-lymphoma-monitoring","kind":"technology","name":"ctDNA monitoring in lymphoma (PhasED-seq, clonoSEQ)","route":"/technologies/ctdna-lymphoma-monitoring/"},{"id":"cytogenetics-fish","kind":"technology","name":"Cytogenetics and FISH","route":"/technologies/cytogenetics-fish/"},{"id":"palliative-care","kind":"technology","name":"Early integrated palliative care","route":"/technologies/palliative-care/"},{"id":"exercise-during-chemotherapy","kind":"technology","name":"Exercise during chemotherapy and radiotherapy","route":"/technologies/exercise-during-chemotherapy/"},{"id":"fdg-pet","kind":"technology","name":"FDG PET","route":"/technologies/fdg-pet/"},{"id":"financial-navigation","kind":"technology","name":"Financial toxicity and financial navigation","route":"/technologies/financial-navigation/"},{"id":"flow-cytometers","kind":"technology","name":"Flow cytometers","route":"/technologies/flow-cytometers/"},{"id":"histopathology-ihc","kind":"technology","name":"Histopathology & immunohistochemistry","route":"/technologies/histopathology-ihc/"},{"id":"checkpoint-inhibitor","kind":"technology","name":"Immune checkpoint inhibitors","route":"/technologies/checkpoint-inhibitor/"},{"id":"clonality-testing","kind":"technology","name":"Immunoglobulin and T-cell receptor clonality testing","route":"/technologies/clonality-testing/"},{"id":"liquid-biopsy","kind":"technology","name":"Liquid biopsy (ctDNA)","route":"/technologies/liquid-biopsy/"},{"id":"monoclonal-antibody","kind":"technology","name":"Monoclonal antibodies","route":"/technologies/monoclonal-antibody/"},{"id":"multidisciplinary-tumour-board","kind":"technology","name":"Multidisciplinary tumour boards","route":"/technologies/multidisciplinary-tumour-board/"},{"id":"flow-cytometry-mrd","kind":"technology","name":"Multiparameter flow cytometry 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