{"entity":{"id":"cdkn2a","kind":"target","name":"CDKN2A","aka":["cyclin dependent kinase inhibitor 2A","Cyclin-dependent kinase inhibitor 2A","CDK4I","p16","INK4a","MTS1","CMM2","p19","p14","INK4","p16INK4a","p19Arf","p14ARF","P16-INK4A","CAI2","CDKN2"],"tldr":"CDKN2A (Cyclin-dependent kinase inhibitor 2A) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Skin cancer, Lung cancer, Bladder & urothelial cancer and 5 more.","summary":"Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.\n\nCIViC holds 59 clinical evidence items and 0 assertions across 27 variants, naming Palbociclib, Trametinib, Afatinib and Bevacizumab and others. Open Targets scores its association with cancer at 0.90 (direct and indirect evidence; datatypes genetic literature 0.61, affected pathway 0.90, literature 1.00, genetic association 0.90, somatic mutation 0.98, animal model 0.67). IntOGen calls it a driver in 70 cohorts (15 activating, 55 loss-of-function), covering Adenoid Cystic Carcinoma, Bladder Urothelial Carcinoma, Invasive Breast Carcinoma, Cholangiocarcinoma, Colon Adenocarcinoma, Colorectal Adenocarcinoma and others. In OnCo, 1 product record names it (UroVysion Bladder Cancer Kit).","asOf":"2026-09-23","links":[{"label":"HGNC HGNC:1787","url":"https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:1787"},{"label":"UniProt P42771","url":"https://www.uniprot.org/uniprotkb/P42771/entry"},{"label":"NCBI Gene 1029","url":"https://www.ncbi.nlm.nih.gov/gene/1029"},{"label":"Ensembl ENSG00000147889","url":"https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000147889"},{"label":"Eskelund et al., Blood 2017: TP53 mutations in 183 younger mantle cell lymphoma patients from Nordic MCL2 and MCL3","url":"https://doi.org/10.1182/blood-2017-04-779736"},{"label":"Rossi et al., Blood 2011: the genetics of Richter syndrome in 86 pathologically proven cases","url":"https://doi.org/10.1182/blood-2010-09-302174"}],"tags":["cancer-genes-wave"],"related":["civic","open-targets","intogen"],"cancers":["skin-cancer","lung-cancer","urothelial","head-and-neck","non-hodgkin-lymphoma","esophageal","leukaemia","ovarian","pancreatic","gallbladder","nsclc"],"sections":[],"technologies":[],"targets":[],"drugs":["urovysion"],"companies":[],"institutions":[],"pathways":["bladder-cancer-signalling","cell-cycle-engine-cdks","cml-signalling","glioma-signalling","hepatocellular-carcinoma-signalling","melanoma-signalling","nsclc-signalling","pancreatic-cancer-signalling","senescence","p53-mdm2-axis","chromosomal-instability"],"terms":["cdkn2a-homozygous-deletion"],"trials":[],"people":[],"bottlenecks":[],"keyPapers":["paper-qian-driver-genes-outcomes-resected-pancreatic-jama-oncol-2018","paper-hu-germline-mutations-pancreatic-cancer-risk-jama-2018","paper-giraldo-gallbladder-msk-impact-ccr-2022","paper-javle-biliary-ngs-cancer-2016","paper-suryavanshi-indian-gallbladder-genomics-jco-go-2025","paper-tcga-lung-squamous-nature-2012"],"journals":[],"dependsOn":[],"notes":["Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: CIViC lists 18 therapies; IntOGen calls it an activating (Act) driver in 15 cohorts; IntOGen calls it a loss-of-function (LoF) driver in 55 cohorts; CIViC holds 59 clinical evidence items on its variants. Evidence tier \"clinical-evidence\" is the strongest of those signals.","Prevalence not recorded: none of the sources gives a positivity rate.","Diseases the sources name that have no OnCo cancer page yet, so they are not linked: Oropharynx Cancer; Supratentorial Ependymoma, ZFTA Fusion-positive; Ganglioglioma; Low-Grade Glioma, NOS.","Pancreatic ductal adenocarcinoma: lost by mutation or deep deletion in 37 to 48%, usually with CDKN2B and often MTAP (deep deletion in 22 to 31% of exome cohorts; cBioPortal). Loss of expression shortened overall survival (19.7 versus 24.6 months) after resection (Qian 2018), and germline CDKN2A carries the highest odds ratio of the six pancreatic risk genes (12.33; Hu 2018). MTAP co-deletion is the entry point for PRMT5-directed agents in trials.","Lung cancer: deep deletion in 15 to 20% of adenocarcinomas and 26.3% of squamous tumours, with mutation on top (cBioPortal); counting methylation and exon skipping as well, CDKN2A and RB1 were altered in 72% of squamous cancers (Cancer Genome Atlas Research Network 2012). The deletion usually takes MTAP with it, which is the entry point for the PRMT5 inhibitors in trials.","Lymphoma, TP53 loss, in mantle cell lymphoma and in Richter transformation: TP53 is the commonest route by which a lymphoma stops responding to chemotherapy, because chemotherapy kills largely by provoking a p53-dependent death. In mantle cell lymphoma it travels with blastoid morphology, a high Ki-67 and CDKN2A deletion. In Richter transformation it is one of two lesions that dominate the genetics, and the transformed clone is usually the same clone as the leukaemia rather than a second cancer. Frequency: In 183 younger mantle cell lymphoma patients from the Nordic MCL2 and MCL3 trials, TP53 mutation in 11% and TP53 deletion in 16%, with CDKN2A deletion in 20% and NOTCH1 mutation in 4%; only TP53 mutation kept its prognostic weight in multivariable analysis, with a hazard ratio of 6.2 for overall survival, a median overall survival of 1.8 years against 12.7 years for unmutated cases, and half the mutated group relapsing within a year (Eskelund 2017). In 86 cases of Richter syndrome, TP53 disruption in 47.1% and MYC abnormality in 26.2%; clonally unrelated transformations had both a longer median survival, 62.5 against 14.2 months, and less TP53 disruption, 23.1% against 60.0% (Rossi 2011). What it changes about treatment: In mantle cell lymphoma, yes in practice if not yet on any label: a TP53 mutation is the usual reason to abandon intensive cytarabine-based induction and autologous transplant and to go to a BTK inhibitor, a BCL-2 inhibitor or CAR-T instead. In Richter transformation it is the main prognostic variable, and establishing whether the large-cell clone is related to the leukaemic one changes the expected outcome more than any drug does."],"provenance":{"editedBy":"scripts/fetch-cancer-genes.ts (CIViC, Open Targets, IntOGen, HGNC, UniProt)","editedOn":"2026-09-23"},"symbol":"CDKN2A","role":["drug-target","oncogene-driver","tumour-suppressor","biomarker"],"evidenceTier":"clinical-evidence","sources":[{"label":"HGNC HGNC:1787","url":"https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:1787","note":"approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)"},{"label":"UniProt P42771","url":"https://www.uniprot.org/uniprotkb/P42771/entry","note":"protein name, function text, keywords and locations (REST API)"},{"label":"CIViC gene CDKN2A","url":"https://civicdb.org/features/14","note":"59 evidence items, 0 assertions, 27 variants; diseases: Head And Neck Squamous Cell Carcinoma, Lung Non-small Cell Carcinoma, Pancreatic Cancer, Melanoma, Cholangiocarcinoma and 20 more (GraphQL API, CC0)"},{"label":"Open Targets ENSG00000147889","url":"https://platform.opentargets.org/target/ENSG00000147889/associations","note":"association with cancer (MONDO_0004992) 0.90; per-cancer scores at or above 0.5: non-small cell lung carcinoma 0.66, gastric cancer 0.58, oesophageal cancer 0.69, hepatocellular carcinoma 0.61, urinary bladder cancer 0.70, ovarian cancer 0.65 (GraphQL API, CC0)"},{"label":"IntOGen CDKN2A","url":"https://www.intogen.org/search?gene=CDKN2A","note":"driver in 70 cohorts (Act 15, LoF 55); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0"}],"specificity":"lineage-antigen","distribution":"many-types","specificityNote":"Lineage antigen shared with normal T-cells: HPA finds the gene group enriched in that blood lineage, and the 1 medicine aimed at it (UroVysion Bladder Cancer Kit) act on the wild-type protein, so the normal lineage is hit too. HPA CDKN2A: RNA tissue enhanced (choroid plexus 43 nTPM, pituitary gland 36 nTPM); blood lineage group enriched (B-cells 16 nTPM, T-cells 38 nTPM); high antibody staining in 3 normal tissues; highest cancer staining cervical cancer (9 of 12 high). Distribution: 9 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Biliary tract cancer (all types), Skin cancer (all types), Lung cancer (all types), Bladder & urothelial cancer, Head and neck squamous cell carcinoma, Lymphoma, Oesophageal cancer and more); Open Targets associates it with 19 specific cancer types at or above 0.5 (dysplastic nevus, familial atypical multiple mole melanoma syndrome, melanoma, cutaneous melanoma, melanoma and neural system tumor syndrome, familial melanoma and more). (Rule 7 of scripts/fetch-target-specificity.ts.)","specificitySources":[{"label":"Human Protein Atlas CDKN2A tissue","url":"https://www.proteinatlas.org/ENSG00000147889-CDKN2A/tissue","note":"RNA tissue and blood lineage specificity, normal tissue antibody staining (version 25.1, CC BY-SA 3.0)"},{"label":"Human Protein Atlas CDKN2A pathology","url":"https://www.proteinatlas.org/ENSG00000147889-CDKN2A/pathology","note":"patients per staining level per cancer type (version 25.1, CC BY-SA 3.0)"},{"label":"Open Targets ENSG00000147889 associations","url":"https://platform.opentargets.org/target/ENSG00000147889/associations","note":"cancer associations at or above 0.5 (CC0)"}],"hgnc":"HGNC:1787","ensembl":"ENSG00000147889","uniprot":"P42771","entrez":"1029","firstDescribed":1993,"firstDescribedBasis":"sequence","firstDescribedNote":"Earliest sequence paper UniProt cites for the protein: Serrano et al, Nature, 1993, \"A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4\".","firstDescribedSource":"https://pubmed.ncbi.nlm.nih.gov/8259215/","biology":"Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein. Location: Cytoplasm; Nucleus (UniProt). Locus 9p21.3 (HGNC).","whereFound":["Skin cancer: Open Targets association 0.80 with skin cancer (MONDO_0002898); IntOGen driver in 1 cohort (SKIN)","Lung cancer: Open Targets association 0.75 with lung cancer (MONDO_0008903)","Bladder & urothelial cancer: Open Targets association 0.70 with urinary bladder cancer (MONDO_0001187); CIViC evidence names this disease","Head and neck squamous cell carcinoma: Open Targets association 0.70 with head and neck squamous cell carcinoma (MONDO_0010150); CIViC evidence names this disease","Non-Hodgkin lymphoma: Open Targets association 0.69 with non-Hodgkin lymphoma (MONDO_0018908); IntOGen driver in 1 cohort (MLYM)","Oesophageal cancer: Open Targets association 0.69 with oesophageal cancer (MONDO_0007576); CIViC evidence names this disease","Pancreatic ductal adenocarcinoma: mutation or deep deletion (with cdkn2b and mtap co-deletion) 37-48%","Gallbladder cancer: deletion or mutation about 21%","Non-small-cell lung cancer: homozygous deletion and inactivating mutation 15-20%","Non-small-cell lung cancer: deletion or mutation of cdkn2a, with rb1 loss 26-41%"],"targetClass":"tumor-suppressor","prevalence":[{"cancerId":"pancreatic","pct":"37-48","measure":"Mutation or deep deletion (with CDKN2B and MTAP co-deletion)","source":"https://www.cbioportal.org/study/summary?id=pdac_msk_2024","note":"cBioPortal: mutation in 546 of 2,336, 23.4%, and deep deletion in 359, 15.4%, in pdac_msk_2024; mutation 35 of 179, 19.6%, and deep deletion 52 of 183, 28.4%, in paad_tcga_pan_can_atlas_2018; mutation 6 and deep deletion 40 of 109, 42.2%, in paad_utsw_2015; mutation 93 of 395, 23.5%, and deep deletion 19 in pancreas_msk_2024; mutation 71 of 383, 18.5%, in paad_qcmg_uq_2016 (no copy-number profile); 29 of 140, 20.7%, in paad_cptac_2021. CDKN2B was co-deleted in 333 of 2,336 (pdac_msk_2024) and 50 of 183 (TCGA); MTAP deep deletion in 40 of 183, 21.9% (TCGA) and 34 of 109, 31.2% (UTSW), 51 of 2,336 on the MSK panel."},{"cancerId":"gallbladder","pct":21,"measure":"Deletion or mutation","source":"https://doi.org/10.1158/1078-0432.ccr-22-1954","note":"CDKN2A 21% (Giraldo 2022); CDKN2A/B 19% of 85 (Javle 2016); CDKN2A 9% of 376 Indian patients, significantly lower than Western and Asian cohorts (Suryavanshi 2025); cBioPortal gbc_mskcc_2022: CDKN2A deep deletion in 35 of 244, 14.3%, mutation in 26 of 244, 10.7%; CDKN2B deep deletion in 34 of 244, 13.9%."},{"cancerId":"nsclc","pct":"15-20","measure":"Homozygous deletion and inactivating mutation","source":"https://www.cbioportal.org/study/summary?id=luad_mskcc_2023_met_organotropism","note":"cBioPortal deep deletion: 358 of 2,422, 14.8%, in luad_mskcc_2023_met_organotropism; 86 of 511, 16.8%, in luad_tcga_pan_can_atlas_2018; 45 of 230, 19.6%, in luad_tcga_pub; 87 of 915, 9.5%, in lung_msk_2017, with mutation on top in 137, 25, 10 and 49 samples respectively."},{"cancerId":"nsclc","pct":"26-41","measure":"Deletion or mutation of CDKN2A, with RB1 loss","source":"https://www.cbioportal.org/study/summary?id=lusc_tcga_pan_can_atlas_2018","note":"cBioPortal: CDKN2A deep deletion 128 of 487, 26.3%, plus mutation in 73 of 484, 15.1%, in lusc_tcga_pan_can_atlas_2018; deletion 47 of 178, 26.4%, plus mutation 31, 17.4%, in lusc_tcga_pub; mutation 17 of 108, 15.7%, in lusc_cptac_2021. RB1 is mutated in 31 of 484, 6.4%, with deep deletion in 16 of 487. The founding paper put CDKN2A and RB1 alteration together at 72% of tumours, counting epigenetic silencing and exon skipping as well as deletion and mutation (Cancer Genome Atlas Research Network 2012)."}]},"route":"/targets/cdkn2a/","neighbours":{"collection":[{"id":"civic","kind":"collection","name":"CIViC","route":"/collections/civic/"},{"id":"intogen","kind":"collection","name":"IntOGen","route":"/collections/intogen/"},{"id":"open-targets","kind":"collection","name":"Open Targets Platform","route":"/collections/open-targets/"}],"cancer":[{"id":"urothelial","kind":"cancer","name":"Bladder & urothelial cancer","route":"/cancers/urothelial/"},{"id":"dlbcl","kind":"cancer","name":"Diffuse large B-cell lymphoma","route":"/cancers/dlbcl/"},{"id":"gallbladder","kind":"cancer","name":"Gallbladder cancer","route":"/cancers/gallbladder/"},{"id":"head-and-neck","kind":"cancer","name":"Head and neck squamous cell carcinoma","route":"/cancers/head-and-neck/"},{"id":"leukaemia","kind":"cancer","name":"Leukaemia (all types)","route":"/cancers/leukaemia/"},{"id":"lung-cancer","kind":"cancer","name":"Lung cancer (all types)","route":"/cancers/lung-cancer/"},{"id":"mantle-cell-lymphoma","kind":"cancer","name":"Mantle cell lymphoma","route":"/cancers/mantle-cell-lymphoma/"},{"id":"non-hodgkin-lymphoma","kind":"cancer","name":"Non-Hodgkin lymphoma (all types)","route":"/cancers/non-hodgkin-lymphoma/"},{"id":"nsclc","kind":"cancer","name":"Non-small-cell lung cancer","route":"/cancers/nsclc/"},{"id":"esophageal","kind":"cancer","name":"Oesophageal cancer","route":"/cancers/esophageal/"},{"id":"ovarian","kind":"cancer","name":"Ovarian cancer","route":"/cancers/ovarian/"},{"id":"pancreatic","kind":"cancer","name":"Pancreatic ductal adenocarcinoma","route":"/cancers/pancreatic/"},{"id":"richter-transformation-cll","kind":"cancer","name":"Richter transformation of chronic lymphocytic leukaemia","route":"/cancers/richter-transformation-cll/"},{"id":"skin-cancer","kind":"cancer","name":"Skin cancer (all types)","route":"/cancers/skin-cancer/"}],"drug":[{"id":"urovysion","kind":"drug","name":"UroVysion Bladder Cancer Kit","route":"/drugs/urovysion/"}],"pathway":[{"id":"bladder-cancer-signalling","kind":"pathway","name":"Bladder cancer (KEGG map)","route":"/pathways/bladder-cancer-signalling/"},{"id":"senescence","kind":"pathway","name":"Cellular senescence","route":"/pathways/senescence/"},{"id":"chromosomal-instability","kind":"pathway","name":"Chromosomal instability & aneuploidy","route":"/pathways/chromosomal-instability/"},{"id":"cml-signalling","kind":"pathway","name":"Chronic myeloid leukaemia (KEGG map)","route":"/pathways/cml-signalling/"},{"id":"glioma-signalling","kind":"pathway","name":"Glioma (KEGG map)","route":"/pathways/glioma-signalling/"},{"id":"hepatocellular-carcinoma-signalling","kind":"pathway","name":"Hepatocellular carcinoma (KEGG map)","route":"/pathways/hepatocellular-carcinoma-signalling/"},{"id":"melanoma-signalling","kind":"pathway","name":"Melanoma (KEGG map)","route":"/pathways/melanoma-signalling/"},{"id":"nsclc-signalling","kind":"pathway","name":"Non-small cell lung cancer (KEGG map)","route":"/pathways/nsclc-signalling/"},{"id":"pancreatic-cancer-signalling","kind":"pathway","name":"Pancreatic cancer (KEGG map)","route":"/pathways/pancreatic-cancer-signalling/"},{"id":"cell-cycle-engine-cdks","kind":"pathway","name":"The cell-cycle engine (cyclins & CDKs)","route":"/pathways/cell-cycle-engine-cdks/"},{"id":"p53-mdm2-axis","kind":"pathway","name":"The p53 network (guardian of the genome)","route":"/pathways/p53-mdm2-axis/"}],"term":[{"id":"cdkn2a-homozygous-deletion","kind":"term","name":"CDKN2A/B homozygous deletion","route":"/terms/cdkn2a-homozygous-deletion/"},{"id":"checkpoint","kind":"term","name":"Checkpoint (two meanings)","route":"/terms/checkpoint/"},{"id":"familial-pancreatic-cancer","kind":"term","name":"Familial pancreatic cancer and inherited risk (who qualifies for surveillance)","route":"/terms/familial-pancreatic-cancer/"},{"id":"lymphoma-bio-lymphgen","kind":"term","name":"LymphGen and the genetic clusters of large B-cell lymphoma","route":"/terms/lymphoma-bio-lymphgen/"},{"id":"panin","kind":"term","name":"Pancreatic intraepithelial neoplasia (PanIN), the microscopic precursor of pancreatic cancer","route":"/terms/panin/"},{"id":"lymphoma-bio-transformation","kind":"term","name":"Transformation: when a slow lymphoma turns into a fast one","route":"/terms/lymphoma-bio-transformation/"}],"paper":[{"id":"paper-springer-pancreatic-cyst-molecular-classification-gastroenterology-2015","kind":"paper","name":"A combination of molecular markers and clinical features improve the classification of pancreatic cysts","route":"/key-papers/paper-springer-pancreatic-cyst-molecular-classification-gastroenterology-2015/"},{"id":"paper-notta-punctuated-evolution-pancreatic-nature-2016","kind":"paper","name":"A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns","route":"/key-papers/paper-notta-punctuated-evolution-pancreatic-nature-2016/"},{"id":"paper-hu-germline-mutations-pancreatic-cancer-risk-jama-2018","kind":"paper","name":"Association Between Inherited Germline Mutations in Cancer Predisposition Genes and Risk of Pancreatic Cancer","route":"/key-papers/paper-hu-germline-mutations-pancreatic-cancer-risk-jama-2018/"},{"id":"paper-qian-driver-genes-outcomes-resected-pancreatic-jama-oncol-2018","kind":"paper","name":"Association of alterations in main driver genes with outcomes of patients with resected pancreatic ductal adenocarcinoma","route":"/key-papers/paper-qian-driver-genes-outcomes-resected-pancreatic-jama-oncol-2018/"},{"id":"paper-javle-biliary-ngs-cancer-2016","kind":"paper","name":"Biliary cancer: utility of next-generation sequencing for clinical management","route":"/key-papers/paper-javle-biliary-ngs-cancer-2016/"},{"id":"paper-skoulidis-kras-co-mutation-subsets-cancer-discov-2015","kind":"paper","name":"Co-occurring genomic alterations define major subsets of KRAS-mutant lung adenocarcinoma with distinct biology, immune profiles, and therapeutic vulnerabilities","route":"/key-papers/paper-skoulidis-kras-co-mutation-subsets-cancer-discov-2015/"},{"id":"paper-tcga-lung-squamous-nature-2012","kind":"paper","name":"Comprehensive genomic characterization of squamous cell lung cancers","route":"/key-papers/paper-tcga-lung-squamous-nature-2012/"},{"id":"paper-giraldo-gallbladder-msk-impact-ccr-2022","kind":"paper","name":"Comprehensive molecular characterization of gallbladder carcinoma and potential targets for intervention","route":"/key-papers/paper-giraldo-gallbladder-msk-impact-ccr-2022/"},{"id":"paper-jones-pancreatic-core-pathways-science-2008","kind":"paper","name":"Core signaling pathways in human pancreatic cancers revealed by global genomic analyses","route":"/key-papers/paper-jones-pancreatic-core-pathways-science-2008/"},{"id":"paper-shindo-germline-sporadic-pancreatic-jco-2017","kind":"paper","name":"Deleterious germline mutations in patients with apparently sporadic pancreatic adenocarcinoma","route":"/key-papers/paper-shindo-germline-sporadic-pancreatic-jco-2017/"},{"id":"paper-bailey-molecular-subtypes-pancreatic-nature-2016","kind":"paper","name":"Genomic analyses identify molecular subtypes of pancreatic cancer","route":"/key-papers/paper-bailey-molecular-subtypes-pancreatic-nature-2016/"},{"id":"paper-jiang-fuscc-tnbc-landscape-cancer-cell-2019","kind":"paper","name":"Genomic and transcriptomic landscape of triple-negative breast cancers: subtypes and treatment strategies","route":"/key-papers/paper-jiang-fuscc-tnbc-landscape-cancer-cell-2019/"},{"id":"paper-suryavanshi-indian-gallbladder-genomics-jco-go-2025","kind":"paper","name":"Genomic profiling of Indian gallbladder carcinoma: mutational insights in a high-incidence population","route":"/key-papers/paper-suryavanshi-indian-gallbladder-genomics-jco-go-2025/"},{"id":"paper-yurgelun-germline-second-hits-resected-pancreatic-genet-med-2019","kind":"paper","name":"Germline cancer susceptibility gene variants, somatic second hits, and survival outcomes in patients with resected pancreatic cancer","route":"/key-papers/paper-yurgelun-germline-second-hits-resected-pancreatic-genet-med-2019/"},{"id":"paper-tcga-pancreatic-integrated-characterisation-cancer-cell-2017","kind":"paper","name":"Integrated genomic characterization of pancreatic ductal adenocarcinoma","route":"/key-papers/paper-tcga-pancreatic-integrated-characterisation-cancer-cell-2017/"},{"id":"paper-caps-consortium-surveillance-recommendations-gut-2020","kind":"paper","name":"Management of patients with increased risk for familial pancreatic cancer: updated recommendations from the International Cancer of the Pancreas Screening (CAPS) Consortium","route":"/key-papers/paper-caps-consortium-surveillance-recommendations-gut-2020/"},{"id":"paper-cowzer-biliary-targeted-therapy-determinants-ccr-2026","kind":"paper","name":"Molecular and clinical determinants of targeted therapy treatment in biliary tract cancer","route":"/key-papers/paper-cowzer-biliary-targeted-therapy-determinants-ccr-2026/"},{"id":"paper-chapuy-molecular-subtypes-dlbcl-nat-med-2018","kind":"paper","name":"Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes","route":"/key-papers/paper-chapuy-molecular-subtypes-dlbcl-nat-med-2018/"},{"id":"paper-biankin-pancreatic-exomes-axon-guidance-nature-2012","kind":"paper","name":"Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes","route":"/key-papers/paper-biankin-pancreatic-exomes-axon-guidance-nature-2012/"},{"id":"paper-kanda-panin-1-somatic-mutations-gastroenterology-2012","kind":"paper","name":"Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia","route":"/key-papers/paper-kanda-panin-1-somatic-mutations-gastroenterology-2012/"},{"id":"paper-singhi-targeted-genome-profiling-3594-pdac-gastroenterology-2019","kind":"paper","name":"Real-time targeted genome profile analysis of pancreatic ductal adenocarcinomas identifies genetic alterations that might be targeted with existing drugs or used as biomarkers","route":"/key-papers/paper-singhi-targeted-genome-profiling-3594-pdac-gastroenterology-2019/"},{"id":"paper-roberts-familial-pancreatic-whole-genome-cancer-discov-2016","kind":"paper","name":"Whole genome sequencing defines the genetic heterogeneity of familial pancreatic cancer","route":"/key-papers/paper-roberts-familial-pancreatic-whole-genome-cancer-discov-2016/"},{"id":"paper-waddell-whole-genomes-pancreatic-nature-2015","kind":"paper","name":"Whole genomes redefine the mutational landscape of pancreatic cancer","route":"/key-papers/paper-waddell-whole-genomes-pancreatic-nature-2015/"}]}}