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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.
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.
Deposited 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.
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.
Shares Andrew J. Aguirre, Broad Institute of MIT and Harvard, Dana-Farber Brigham Cancer Center, RNA sequencing & expression profiling.
Shares SMAD4, CDKN2A, Dana-Farber Brigham Cancer Center, RAS / RAF / MEK / ERK (MAPK).
Shares Wild-type (WT), KRAS wild-type pancreatic ductal adenocarcinoma, RNA sequencing & expression profiling, Whole-exome & whole-genome sequencing.
Shares Wild-type (WT), KRAS wild-type pancreatic ductal adenocarcinoma, RNA sequencing & expression profiling, Whole-exome & whole-genome sequencing.