Year: 2012
Type: article
Abstract: Experts have long appreciated that the clinical entity we call colorectal cancer is a phenotype made up of numerous different genotypes, accounting for the wide variation in clinical course and responses to therapies experienced by different individuals.Observations reported by Khambata-Ford et al 1 and subsequently confirmed by Amado et al 2 have made the practicing community aware that activating mutations in exon 2 of the gene encoding for KRAS, a key signal transduction protein, result in primary resistance to anti-epidermal growth factor receptor (EGFR) agents by leading to EGFR-independent activation of mitogen-activated protein kinase (MAPK) signaling.BRAF is a signal transduction protein that is downstream of KRAS in the MAPK pathway.Approximately 5% to 10% of colorectal cancers harbor mutations in BRAF; the most common is the V600E mutation.The occurrence of these mutations in colorectal cancers raises 2 important questions: what are the clinical characteristics of a colorectal cancer with a V600E BRAF mutation, and can that mutation be targeted for therapeutic advantage?
Authors: Rona Yaeger, Leonard Saltz
Institution: Memorial Sloan Kettering Cancer Center
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2171750041