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402812 | New Interpretation | 01/22/2019 1:41 PM |
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Tier 2InterpretationKRAS, member of the RAS family of small GTPases which functions as an upstream regulator of the MAPK and PI3K pathways, is frequently mutated in a diverse range of cancers including pancreatic, colorectal and lung cancers. More than 90% of pancreatic ductal adenocarcinoma samples have a KRAS mutation which may have prognostic, and (with ongoing trials assessing the efficacy of novel KRAS inhibitors) possibly therapeutic implications. However, targeting KRAS directly has been difficult in these tumors. KRAS mutations are infrequent in gastric carcinomas and have been reported in approximately 6% of cases. The gain of function KRAS G12D mutation is known to be oncogenic.
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Citations- Ahearn IM, Haigis K, Bar-Sagi D, Philips MR. Regulating the regulator:post-translational modification of RAS. Nat Rev Mol Cell Biol. 2011 Dec 22;13(1):39-51.
- Eser et al.. Oncogenic KRAS signaling in pancreatic cancer. British Journal of Cancer (2014) 111, 817--822
- van Grieken NC, et al. KRAS and BRAF mutations are rare and related to DNA mismatch repair deficiency in gastric cancer from the East and the West: results from a large international multicentre study. Br J Cancer. 2013 Apr 16;108(7):1495-501.
- Park SR, et al. Predictive factors for the efficacy of cetuximab plus chemotherapy as salvage therapy in metastatic gastric cancer patients. Cancer Chemother Pharmacol. 2010 Feb;65(3):579-87.
- Queiros P, et al. KRAS mutations in microsatellite instable gastric tumours: impact of targeted treatment and intratumoural heterogeneity. Virchows Arch 2015;467(4):383-92.
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Last updated: 2019-01-22 18:41:07 UTC
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