Relevance of MET activation and genetic alterations of KRAS and E-cadherin for cetuximab sensitivity of gastric cancer cell lines

Abstract

These data indicate that our examinations may be clinically relevant, and the candidate markers should therefore be tested in clinical studies.

Biomarker analysis in oesophagogastric cancer: Results from the REAL3 and TransMAGIC trials

“…10,13,27,28 This contrasts the effect of KRAS mutations in mCRC 4,29,30 ; possibly due to the small sample sizes of the oesophagogastric trials and relative rarity of KRAS, BRAF and PIK3CA mutations 31,32 It is, therefore, plausible that these uncommon mutations do confer resistance to anti-EGFR antibodies in oesophagogastric cancer, but that this effect has been masked by both the low prevalence of the mutations and co-administration with chemotherapy.…”

KRAS status and resistance to epidermal growth factor receptor tyrosine‐kinase inhibitor treatment in patients with metastatic colorectal cancer: a meta‐analysis

“…It can regulate biological cellular responses such as tumour proliferation, survival and differentiation [24]. Mutations in downstream signalling effectors of EGFR could result in resistance to EGFR inhibitors [25][26][27]. In mCRC, the most frequently detected alterations in EGFR signalling pathways are KRAS mutations.…”

Predictive Biomarker Candidates for The Response Of Gastric Cancer to Targeted And Cytotoxic Agents

“…Thus, KRAS and BRAF mutations have not been fully evaluated as predictive markers of EGFR-targeted therapy in gastric cancer patients. Activating mutations and amplification of KRAS confer resistance to EGFR inhibitors and also to mTOR and MET inhibition in colon and gastric cancer cells [33][34][35]. Thus, collaborative groups should perform largescale biomarker studies to evaluate the predictive role of KRAS activation for resistance to targeted therapies and to develop strategies to therapeutically target KRAS.…”