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Karapetis, Christos S; Khambata-Ford, Shirin; Jonker, Derek J; O'Callaghan, Chris J; Tu, Dongsheng; Tebbutt, Niall C; Simes, R. John; Chalchal, Haji; Shapiro, Jeremy D; Robitaille, Sonia; Price, Timothy J; Shepherd, Lois; Au, Heather-Jane; Langer, Christiane; Moore, Malcolm J; Zalcberg, John R
The New England journal of medicine, 10/2008, Volume: 359, Issue: 17Journal Article
This study examined the mutation status of the K-ras gene in colorectal tumors from patients who were enrolled in a trial of cetuximab, a monoclonal antibody against the epidermal growth factor receptor (EGFR). A survival benefit was found among patients with tumors bearing wild-type K-ras but not among patients with tumors bearing mutated K-ras . Wild-type K-ras is essential in transmitting signals initiated by EGFR. This study examined the mutation status of the K-ras gene in colorectal tumors from patients who were enrolled in a trial of cetuximab. A survival benefit was found among patients with tumors bearing wild-type K-ras but not among patients with tumors bearing mutated K-ras . A randomized trial (CO.17) conducted by the National Cancer Institute of Canada Clinical Trials Group (NCIC CTG) in collaboration with the Australasian Gastro-Intestinal Trials Group (AGITG) showed that among patients with colorectal cancer that had not responded to advanced chemotherapy, monotherapy with cetuximab, a monoclonal antibody directed against the epidermal growth factor receptor (EGFR), improved overall survival and progression-free survival and preserved the quality of life better than did best supportive care alone. 1 However, resistance to cetuximab was common: at the first assessment of disease response, the disease had progressed in more than 50% of treated patients. K-ras , a . . .
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