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lymph nodes,” Dr. Boland said. Patients need to be tested for BRAF mutation status, staged appropriately, and surgically managed (wide excision, LND), with consideration given to enrolling appropriate patients in neoadjuvant trials. Adjuvant

5% to 9% of CRCs are characterized by a specific mutation in the BRAF gene (V600E). 32 , 33 BRAF mutations are, for all practical purposes, limited to tumors that do not have KRAS exon 2 mutations. 32 – 34 The NCCN panel currently recommends

molecularly selective settings. The targeting of the RAS/RAF/MEK/ERK pathway with clinically available surrogate markers harboring KRAS and/or BRAF mutations could be a strategy for selecting more responsive personalized cancer therapy using molecular

overall survival according to tumor KRAS and BRAF mutation status . J Clin Oncol 2011 ; 29 : 2011 – 2019 . 10 Douillard JY Siena S Cassidy J . Randomized, phase III trial of panitumumab with infusional fluorouracil, leucovorin, and

trial, 675 patients with metastatic melanoma and BRAF mutation (as detected with the COBAS 4800 V600E mutation test) were randomized to vemurafenib (960 mg orally, twice daily) versus dacarbazine (1000 mg/kg every 3 weeks). 12 The hazard ratio for

KIT gene are the most common, accounting for 80% to 85% of GIST mutations, with PDGFR α mutations representing 5% to 10% of mutations. The remaining mutations have been termed wild-type ; however, SDH and BRAF mutations have been identified

from epigenetic hypermethylation of the hMLH1 promoter, and also typically showing BRAF mutation) are worth detecting because of differences in prognosis and response to adjuvant therapies that include 5-FU. 14 This is the position of the EGAPP. 15

hypermethylation, whereas absence of the BRAF mutation suggests a germline mutation in MLH1, and thus LS. Depending on the population and study design, the percentage of carcinomas that show loss of DNA MMR protein expression is approximately 15% (and reported

cases, an assay directed at detecting MLH-1 hypermethylation or its surrogate, BRAF mutation, may suggest the non-HNPCC/LS basis and a recommendation for no further HNPCC/LS-related testing. MSI/IHC testing is now often routine and does not require

and acquired BRAF mutations as potential mechanisms of resistance, both of which have potential therapeutic implications that will require further study. 23 , 24 Second-Generation EGFR TKIs Acquired resistance to first-generation EGFR TKIs