Cancer Cell is Cell Press's dedicated cancer journal, publishing mechanism-rich papers on tumour biology, the microenvironment, resistance and biomarkers, plus the CPTAC proteogenomic atlases.
Cancer Cell is Cell Press's dedicated cancer journal, founded in 2002, appearing monthly and published by Cell Press (Elsevier) on a hybrid model. It publishes mechanism-rich papers on tumour biology, the microenvironment, drug resistance and biomarkers, including multi-omic studies such as the CPTAC proteogenomic atlases and TCGA subtype papers and translational biomarker work that often accompanies clinical trials. Its readers are cancer biologists and translational researchers. Within OnCo it is related to the CPTAC consortium and the Cancer Cell source feed and is linked from the biographies of Rui-Hua Xu, Ross Levine, Aaron Schimmer, Frank McCormick, Lajos Pusztai and Michael Taylor, and it is where a reader would look for the mechanistic paper behind a resistance story.
This is the paper Europe PMC returns for registry id NCT05890742 with the most citations, so it is the natural first reading for anyone following the dMMR Resectable Colon Cancer trial. Read the abstract above alongside the trial page and the registry entry; the record was linked automatically and its figures have not been checked by hand.
One pathway page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
One trial page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
It offers the first credible explanation for why only a minority of small-cell patients get a durable benefit from checkpoint blockade, and it introduces subtype switching, which would mean retesting at relapse rather than typing once.
The piece that turns a research classification into something a trial can use on one person's biopsy, with a probability attached rather than a flat label. It is the reason genetics-directed lymphoma trials became possible at all.
The clearest statement of why the corpus records so many negative immunotherapy trials here, and of the design logic behind the vaccine and agonist combinations now in trials.
The FUSCC cohort is the East Asian reference and the basis of the FUTURE subtype-guided umbrella trial; its LAR findings point to CDK4/6 and HER2-mutant strategies rather than PARP inhibitors for that subtype.
One of the most cited papers Europe PMC returns for E. Shelley Hwang at Duke Cancer Institute, so it is a natural starting point for reading their work. The record was linked automatically from the author list and affiliation; read the abstract above and the paper itself before relying on any figure.
It turned sidedness from an epidemiological curiosity into a mechanistic statement, and it is the reason a wild-type mitogenic report on a left-sided tumour is read as ligand dependence rather than as an absence.
One idea page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
It gives the 3 to 4% of KDM6A-mutant, squamous-programme tumours a mechanism and a candidate drug class.
It shows that leaving androgen receptor dependence does not have to mean becoming neuroendocrine, and it names a treatable pathway for a group of men whose tumours would otherwise be described only by what they lack.
It is the reference multi-platform dataset and the reason a KRAS wild-type report is treated as a search for another driver rather than as an absence.
The 2021 WHO paediatric-type diffuse high-grade glioma categories, and the practice of profiling every childhood glioma for a targetable fusion or mutation, rest on this landscape.
Subtype-level classification, particularly separating infant and TP53-mutant SHH tumours and MYC-amplified group 3 tumours, guides current risk stratification and trial design.
One cancer page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
One term page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
Together with the negative HALO-301 trial of hyaluronidase this ended the first, blunt version of stromal targeting; second-generation ideas aim to reprogramme rather than remove the stroma.
One of the most cited papers Europe PMC returns for E. Shelley Hwang at Duke Cancer Institute, so it is a natural starting point for reading their work. The record was linked automatically from the author list and affiliation; read the abstract above and the paper itself before relying on any figure.
Published alongside Ozdemir, it explains why the hedgehog inhibitor trials in patients failed and why stromal targets are now chosen for their signalling rather than their bulk.
Chromophobe renal cell carcinoma is a biologically distinct disease that should not be lumped with clear cell cancer in trials or treatment, which is why its page separates the two.
One term page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
It is the reason every prostate PI3K or AKT trial gives the drug with abiraterone rather than alone, and the reason PTEN loss is used to select for those combinations rather than as a general prognostic marker.
The origin of the idea that a prostate tumour's copy-number pattern carries prognostic information the pathologist's grade does not. That idea became Decipher and the other genomic classifiers, which are now used in some systems to decide whether a man needs radiotherapy after surgery.
One term page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
One term page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
Leukaemia researcher who found that AML stem cells depend on mitochondrial proteases and metabolism.
Cancer biologist who has been President and CEO of The Wistar Institute in Philadelphia since 2015 and directs its NCI-designated Ellen and Ronald Caplan Cancer Center.
Duke surgeon who led COMET, the trial testing whether women with low-risk DCIS can safely be monitored instead of having surgery straight away.
RAS biologist who founded Onyx Pharmaceuticals and led the NCI's national effort to drug RAS.
H.M.W. Verheul represents Erasmus MC Cancer Institute in the Organisation of European Cancer Institutes, which lists the centre among its members in The Netherlands.
Paris paediatric neuro-oncologist who led HERBY, the trial that showed adding bevacizumab does not help children with high-grade glioma, and who leads European trials in diffuse midline glioma.
Cell signalling scientist who has been President and Scientific Director of the Terry Fox Research Institute, the research arm of The Terry Fox Foundation, since 2021.
Tumour immunologist at Ludwig Lausanne who began a two-year term as President of the European Association for Cancer Research in June 2026.
Medicinal chemist who led the discovery of the proteasome inhibitor bortezomib and now heads Stand Up To Cancer as President and CEO.
Translational breast oncologist who co-leads the I-SPY2 platform trial and helped show immunotherapy works in early TNBC.
Medical oncologist and cancer biologist at Tübingen, known for work on senescence surveillance and functional genomics in liver cancer.
Paediatric oncologist and neuroblastoma researcher who leads Children's Cancer Institute in Sydney, Australia's dedicated childhood cancer research institute.
Neurosurgeon-scientist who defined the four molecular subgroups of medulloblastoma that now guide therapy.
Glasgow cancer biologist who directs the CRUK Scotland Institute and is Scientific Director of the CRUK Scotland Centre, known for mouse models of colorectal and pancreatic cancer.
Discovered the JAK2 mutation behind most myeloproliferative neoplasms and defined the genetics of clonal haematopoiesis.
Leads China's largest cancer centre and has run the Chinese phase 3 trials that brought PD-1 antibodies into GI cancer.
Directs the translational research department that developed models and targets for uveal melanoma.
Shaomeng Wang is the medicinal chemist behind some of the first clinical MDM2 inhibitors and PROTAC degraders.
Haematologist and Senior Group Leader at CRUK Manchester Institute studying the transcriptional drivers of acute myeloid leukaemia.
Genome biologist who chairs UMC Utrecht's Strategic Program Cancer, the umbrella for more than 800 cancer researchers in Utrecht.
Co-architect of the Fudan TNBC subtypes and the metabolic and immune atlases that guide subtype-specific treatment.
Leads the world's highest-volume breast cancer surgical unit and the FUTURE trial that treats triple-negative breast cancer by molecular subtype.
This is the paper Europe PMC returns for registry id NCT05890742 with the most citations, so it is the natural first reading for anyone following the dMMR Resectable Colon Cancer trial. Read the abstract above alongside the trial page and the registry entry; the record was linked automatically and its figures have not been checked by hand.
One pathway page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
One trial page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
It offers the first credible explanation for why only a minority of small-cell patients get a durable benefit from checkpoint blockade, and it introduces subtype switching, which would mean retesting at relapse rather than typing once.
The piece that turns a research classification into something a trial can use on one person's biopsy, with a probability attached rather than a flat label. It is the reason genetics-directed lymphoma trials became possible at all.
The clearest statement of why the corpus records so many negative immunotherapy trials here, and of the design logic behind the vaccine and agonist combinations now in trials.
The FUSCC cohort is the East Asian reference and the basis of the FUTURE subtype-guided umbrella trial; its LAR findings point to CDK4/6 and HER2-mutant strategies rather than PARP inhibitors for that subtype.
One of the most cited papers Europe PMC returns for E. Shelley Hwang at Duke Cancer Institute, so it is a natural starting point for reading their work. The record was linked automatically from the author list and affiliation; read the abstract above and the paper itself before relying on any figure.
Shares Human Tumor-Associated Macrophage and Monocyte Transcriptional Landscapes Reveal Cancer-Specific Reprogramming, Biomarkers, and Therapeutic Targets, Macrophage IL-10 blocks CD8+ T cell-dependent responses to chemotherapy by suppressing IL-12 expression in intratumoral dendritic cells.
Shares Toripalimab plus chemotherapy in treatment-naïve, advanced esophageal squamous cell carcinoma (JUPITER-06): A multi-center phase 3 trial, Rui-Hua Xu.
Shares Antiangiogenesis strategies revisited: from starving tumors to alleviating hypoxia, Tensional homeostasis and the malignant phenotype.