{"entity":{"id":"paper-tcga-pancreatic-integrated-characterisation-cancer-cell-2017","kind":"paper","name":"Integrated genomic characterization of pancreatic ductal adenocarcinoma","aka":[],"tldr":"The Cancer Genome Atlas profiled 150 pancreatic cancers on every platform, confirmed the driver list, showed that tumours without a KRAS mutation carry other growth-signal drivers such as GNAS, BRAF and CTNNB1, and found some tumours with two KRAS mutations.","summary":"Integrated genomic, transcriptomic and proteomic profiling of 150 pancreatic ductal adenocarcinoma specimens, including samples with characteristically low neoplastic cellularity. Deep whole-exome sequencing revealed recurrent somatic mutations in KRAS, TP53, CDKN2A, SMAD4, RNF43, ARID1A, TGFBR2, GNAS, RREB1 and PBRM1. KRAS wild-type tumours harboured alterations in other oncogenic drivers including GNAS, BRAF, CTNNB1 and additional RAS pathway genes. A subset of tumours harboured multiple KRAS mutations, some biallelic. Protein profiling identified a favourable-prognosis subset with low epithelial-mesenchymal transition and high MTOR pathway scores.\n\nDeposited as paad_tcga_pan_can_atlas_2018 on cBioPortal with 184 samples, including the low-cellularity and non-ductal samples excluded from the 150-tumour analysis; KRAS reads 117 of 179 sequenced there for that reason.","asOf":"2026-09-24","links":[{"label":"Cancer Genome Atlas Research Network, Cancer Cell 2017: integrated characterisation of 150 pancreatic ductal adenocarcinomas","url":"https://doi.org/10.1016/j.ccell.2017.07.007"},{"label":"PubMed","url":"https://pubmed.ncbi.nlm.nih.gov/28810144/"},{"label":"cBioPortal study paad_tcga_pan_can_atlas_2018 (TCGA PanCancer Atlas; 184 samples, 179 sequenced, 183 with copy number; the deposit keeps the low-cellularity and non-ductal samples the 2017 paper excluded)","url":"https://www.cbioportal.org/study/summary?id=paad_tcga_pan_can_atlas_2018"}],"tags":[],"related":[],"cancers":["pancreatic","kras-wild-type-pdac"],"sections":[],"technologies":["wes-wgs","rna-seq","proteomics"],"targets":["kras","tp53","cdkn2a","smad4","rnf43","arid1a","tgfbr2","gnas","braf","ctnnb1"],"drugs":[],"companies":[],"institutions":["nci","broad-institute","dana-farber"],"pathways":["pancreatic-cancer-signalling","ras-mapk"],"terms":["wild-type"],"trials":[],"people":["andrew-aguirre"],"bottlenecks":[],"keyPapers":[],"journals":["cancer-cell"],"dependsOn":[],"notes":[],"journal":"Cancer Cell","year":2017,"doi":"10.1016/j.ccell.2017.07.007","pmid":"28810144","authors":"Cancer Genome Atlas Research Network (Raphael BJ, Hruban RH, Aguirre AJ, et al.).","paperType":"translational","findings":["Recurrent mutations: KRAS, TP53, CDKN2A, SMAD4, RNF43, ARID1A, TGFBR2, GNAS, RREB1, PBRM1.","KRAS wild-type tumours carry GNAS, BRAF, CTNNB1 or other RAS pathway drivers.","A subset carries multiple, sometimes biallelic, KRAS mutations."],"whatItMeans":"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.","caveats":["Low cellularity required purity-aware analysis; the public deposit is not the analysed set.","Subtype calls on bulk tissue depend on the classifier."],"changedPractice":false,"participants":150},"route":"/key-papers/paper-tcga-pancreatic-integrated-characterisation-cancer-cell-2017/","neighbours":{"cancer":[{"id":"kras-wild-type-pdac","kind":"cancer","name":"KRAS wild-type pancreatic ductal adenocarcinoma","route":"/cancers/kras-wild-type-pdac/"},{"id":"pancreatic","kind":"cancer","name":"Pancreatic ductal adenocarcinoma","route":"/cancers/pancreatic/"}],"technology":[{"id":"proteomics","kind":"technology","name":"Proteomics & phosphoproteomics","route":"/technologies/proteomics/"},{"id":"rna-seq","kind":"technology","name":"RNA sequencing & expression profiling","route":"/technologies/rna-seq/"},{"id":"wes-wgs","kind":"technology","name":"Whole-exome & whole-genome sequencing","route":"/technologies/wes-wgs/"}],"target":[{"id":"arid1a","kind":"target","name":"ARID1A","route":"/targets/arid1a/"},{"id":"braf","kind":"target","name":"BRAF","route":"/targets/braf/"},{"id":"cdkn2a","kind":"target","name":"CDKN2A","route":"/targets/cdkn2a/"},{"id":"ctnnb1","kind":"target","name":"CTNNB1","route":"/targets/ctnnb1/"},{"id":"gnas","kind":"target","name":"GNAS","route":"/targets/gnas/"},{"id":"kras","kind":"target","name":"KRAS","route":"/targets/kras/"},{"id":"rnf43","kind":"target","name":"RNF43","route":"/targets/rnf43/"},{"id":"smad4","kind":"target","name":"SMAD4","route":"/targets/smad4/"},{"id":"tgfbr2","kind":"target","name":"TGFBR2","route":"/targets/tgfbr2/"},{"id":"tp53","kind":"target","name":"TP53","route":"/targets/tp53/"}],"institution":[{"id":"broad-institute","kind":"institution","name":"Broad Institute of MIT and Harvard","route":"/institutions/broad-institute/"},{"id":"dana-farber","kind":"institution","name":"Dana-Farber Brigham Cancer Center","route":"/institutions/dana-farber/"},{"id":"nci","kind":"institution","name":"National Cancer Institute (NIH)","route":"/institutions/nci/"}],"pathway":[{"id":"pancreatic-cancer-signalling","kind":"pathway","name":"Pancreatic cancer (KEGG map)","route":"/pathways/pancreatic-cancer-signalling/"},{"id":"ras-mapk","kind":"pathway","name":"RAS / RAF / MEK / ERK (MAPK)","route":"/pathways/ras-mapk/"}],"term":[{"id":"wild-type","kind":"term","name":"Wild-type (WT)","route":"/terms/wild-type/"}],"person":[{"id":"andrew-aguirre","kind":"person","name":"Andrew J. Aguirre","route":"/people/andrew-aguirre/"}],"journal":[{"id":"cancer-cell","kind":"journal","name":"Cancer Cell","route":"/journals/cancer-cell/"}]}}