PNAS is the US National Academy of Sciences' weekly multidisciplinary journal, free to read six months after publication. Its cancer landmarks include the early oncogene and tumour-suppressor papers, the first PROTAC concept paper and the Iwai and Honjo paper showing that tumours use PD-L1 to escape T cells.
The Proceedings of the National Academy of Sciences (PNAS) is the multidisciplinary journal of the US National Academy of Sciences, founded in 1915, appearing weekly and available on a hybrid model with free access after six months. It publishes across all sciences, and its cancer landmarks include early oncogene, tumour-suppressor and cancer-evolution modelling papers, mutational-signature methods, and statistical work on cancer risk and screening. Its readers are scientists of every discipline, which is why foundational cancer biology often appeared here. Within OnCo it is the journal of the first PROTAC concept paper and of the Iwai and Honjo paper showing that tumours use PD-L1 to escape T cells, and a reader would use it for foundational cancer biology and modelling work.
It is the most disciplined outcome analysis in this disease and its result is deflationary in a useful way: most of the alterations people quote as prognostic do not survive adjustment, and the one that does, RB1, is also the one that marks the route to neuroendocrine transformation.
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.
It quantifies how little DNA an operable pancreatic cancer sheds and why every serious early detection panel pairs DNA with proteins.
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.
This is the evidence base for offering an inherited-risk test to a whole population rather than to people who already look high risk. It is why Israel's health basket funds BRCA founder testing for every woman of Ashkenazi origin without a family history requirement, and it is quoted in every argument for doing the same elsewhere.
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.
The mechanistic account of T-cell exclusion that all later combination immunotherapy trials in pancreatic cancer cite, and the origin of CXCR4 inhibitor combinations.
One technology 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 put RNF43 on the pancreatic driver list and gave cyst fluid testing a way to separate the harmless serous cyst from the mucinous ones that need watching.
MYB immunostaining and MYB-NFIB fusion testing are now diagnostic tools for adenoid cystic carcinoma, and MYB is the principal target of therapeutic research in the disease.
This paper extended the cancer stem cell concept from leukaemia to a common solid tumour and started the search for tumour-initiating cells across cancers. It underpins research on why cancers relapse after treatments that shrink them and on therapies aimed at the cells that regrow disease.
The molecular bridge between germline BRCA1 and triple-negative breast cancer; it is why every triple-negative patient under 60 is now offered germline testing and why PARP inhibitors were tried in this disease first.
Tumours hide from T cells by displaying PD-L1; blocking that interaction lets the immune system attack. This is the mechanism of pembrolizumab, nivolumab, atezolizumab and their relatives, which now treat more than 20 cancer types.
The first evidence that the basal-like group is not just biologically distinct but clinically dangerous, the observation that triple-negative outcome studies of 2007 confirmed in the clinic.
Instead of blocking a cancer protein, a drug can now remove it entirely, which works even for proteins without a druggable active site and can overcome resistance driven by target overexpression or mutation. Several degraders are in late-stage trials for breast and prostate cancer.
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 established the epigenetic route to mismatch repair deficiency, which is why an MLH1-deficient tumour is tested for MLH1 methylation or BRAF V600E before a family is told it may have Lynch syndrome.
Every approved CAR-T product descends from this design. It is the reason a T cell can be pointed at CD19 or BCMA at all, and the reason the question of what to point it at in solid tumours is a question about antigens rather than about the receptor.
The seroepidemiology that tied a virus to a cancer across a population rather than in one patient. It is the reason blood donations are screened for human T-lymphotropic virus type 1 in Japan and elsewhere, and the reason breastfeeding advice is part of cancer prevention in endemic regions.
The first human retrovirus, and the start of the line of work that identified HIV three years later. For lymphoma it means that adult T-cell leukaemia/lymphoma has a known, transmissible, preventable cause, and that screening blood donors and advising on breastfeeding in endemic areas are cancer prevention measures.
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.
Geneticist known for work on the genetic drivers of childhood brain cancer who became Director and CEO of QIMR Berghofer, a leading Australian medical research institute, in 2026.
Pulmonologist appointed Superintendent of National Taiwan University Hospital in August 2025, leading Taiwan's flagship academic medical centre.
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.
Co-developed the HPV vaccine technology that is eliminating cervical cancer in vaccinated populations.
Immunologist who helped define the PD-1 pathway's role in cancer and built one of the largest immunotherapy institutes.
Produced the evidence that made Israel the first country to offer BRCA testing to a whole population group, by measuring cancer risk in carriers found through healthy men rather than through cancer clinics.
Biologist and long-time CNIO director of biotechnology programmes who became Acting Scientific Director of Spain's national cancer research centre in 2025.
Leads Japan's national cancer centre, the hub of the country's genomic medicine and early-phase trial programmes.
Isolated the first blood stem cells and discovered the 'don't eat me' signal CD47 on cancer cells.
Discovered that blocking CTLA-4 unleashes T cells against cancer, the work behind ipilimumab and the 2018 Nobel Prize.
DNA repair scientist who directs the Fred & Pamela Buffett Cancer Center in Omaha and the UNMC Eppley Institute.
Immunologist who studies why tumours resist immunotherapy and directs the Goodman Cancer Institute, McGill University's cancer research institute in Montreal.
Discovered PD-L1 (B7-H1) and showed tumours use it to escape immunity, the biology behind every anti-PD-1 drug.
Stem cell biologist who directs BRIC-inStem in Bengaluru, India's national institute for stem cell science and regenerative medicine.
Max Wicha identified breast cancer stem cells and made them a therapeutic target.
Cloned p53 and then spent a career on what it does. The field's first reading of his own 1984 result, that p53 was an oncogene, turned out to be wrong, and the correction is the better story.
Engineer who founded and directs the Cancer Center at Illinois, the University of Illinois Urbana-Champaign centre that applies engineering and basic science to cancer.
Saijuan Chen helped turn acute promyelocytic leukaemia from a leukaemia that often killed within weeks into one of the most curable, by showing how retinoic acid and arsenic act and combining them.
Cancer biologist turned research executive who serves as CEO of the ANZUP Cancer Trials Group.
He discovered the PD-1 molecule on T cells in 1992 and showed it acts as a brake on immune attack. Blocking it produced nivolumab and pembrolizumab, now used across dozens of cancers; Nobel Prize 2018.
One of the people who worked out what the HER family of receptors does and how antibodies against them behave, including why combining two antibodies against the same receptor works better than either alone.
The immunologist who, in 1989, first gave a T cell an antibody's aim. Every CAR-T product on the market descends from that experiment.
Zhu Chen, a leukaemia scientist who became China's health minister, co-developed the retinoic acid plus arsenic treatment that cures most acute promyelocytic leukaemia and then reformed the health system that pays for it.
It is the most disciplined outcome analysis in this disease and its result is deflationary in a useful way: most of the alterations people quote as prognostic do not survive adjustment, and the one that does, RB1, is also the one that marks the route to neuroendocrine transformation.
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.
It quantifies how little DNA an operable pancreatic cancer sheds and why every serious early detection panel pairs DNA with proteins.
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.
This is the evidence base for offering an inherited-risk test to a whole population rather than to people who already look high risk. It is why Israel's health basket funds BRCA founder testing for every woman of Ashkenazi origin without a family history requirement, and it is quoted in every argument for doing the same elsewhere.
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.
The mechanistic account of T-cell exclusion that all later combination immunotherapy trials in pancreatic cancer cite, and the origin of CXCR4 inhibitor combinations.
Shares Altered interactions between unicellular and multicellular genes drive hallmarks of transformation in a diverse range of solid tumors, Ancestral gene regulatory networks drive cancer.
Shares Mutation and cancer: statistical study of retinoblastoma, Normal genetically mosaic mice produced from malignant teratocarcinoma cells, Tumour suppressor gene.
Shares Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications, Repeated observation of breast tumor subtypes in independent gene expression data sets.
Shares Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications, Repeated observation of breast tumor subtypes in independent gene expression data sets.
Shares Adult T-cell leukemia: antigen in an ATL cell line and detection of antibodies to the antigen in human sera, Detection and isolation of type C retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma.
Shares Whole-exome sequencing of neoplastic cysts of the pancreas reveals recurrent mutations in components of ubiquitin-dependent pathways, Combined circulating tumor DNA and protein biomarker-based liquid biopsy for the earlier detection of pancreatic cancers, Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma.
Shares Adult T-cell leukemia: antigen in an ATL cell line and detection of antibodies to the antigen in human sera, Detection and isolation of type C retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma.