2017
DOI: 10.1016/j.ccell.2017.07.007
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Abstract: SUMMARY We performed integrated genomic, transcriptomic and proteomic profiling of 150 pancreatic ductal adenocarcinoma (PDAC) specimens, including samples with characteristic low neoplastic cellularity. Deep whole-exome sequencing revealed recurrent somatic mutations in KRAS, TP53, CDKN2A, SMAD4, RNF43, ARID1A, TGFβR2, GNAS, RREB1 and PBRM1. KRAS wild-type tumors harbored alterations in other oncogenic drivers, including GNAS, BRAF, CTNNB1 and additional RAS pathway genes. A subset of tumors harbored multiple… Show more

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Cited by 1,332 publications
(1,010 citation statements)
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“…The recent characterization of the genomic landscape of PDAC [13,14,15,16,17,18] has spurred an increased interest in the development of targeted therapeutic approaches to tackle this disease. Given this dominance of KRAS mutations among the known driver lesions in PDAC, we provide a brief overview on the various approaches to therapeutically target oncogenic KRAS.…”
Section: Targeting Oncogenic Krasmentioning
confidence: 99%
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“…The recent characterization of the genomic landscape of PDAC [13,14,15,16,17,18] has spurred an increased interest in the development of targeted therapeutic approaches to tackle this disease. Given this dominance of KRAS mutations among the known driver lesions in PDAC, we provide a brief overview on the various approaches to therapeutically target oncogenic KRAS.…”
Section: Targeting Oncogenic Krasmentioning
confidence: 99%
“…These large-scale sequencing efforts revealed that approximately 90% of PDAC cases harbor oncogenic KRAS mutations, which in the majority of the cases co-cluster with pathogenic TP53 mutations [18]. The importance of the KRAS-MAPK pathway in PDAC is further underlined by the observation that KRAS wild-type tumors frequently harbor mutations in additional RAS pathway members, as well as aberrations in GNAS , BRAF and CTNNB1 [18]. …”
Section: Introductionmentioning
confidence: 99%
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