English Version
Abstract
Background
Fluoropyrimidine based chemotherapy plus the anti vascular endothelial growth factor (VEGF) antibody bevacizumab is standard firstline treatment for metastatic colorectal cancer. We studied the ef fect of adding the ant i-epidermal growth factor receptor (EGFR) antibody cetuximab to a combination of capecitabine, oxaliplatin, and bevacizumab for metastatic colorectal cancer.
Background
Fluoropyrimidine based chemotherapy plus the anti vascular endothelial growth factor (VEGF) antibody bevacizumab is standard firstline treatment for metastatic colorectal cancer. We studied the ef fect of adding the ant i-epidermal growth factor receptor (EGFR) antibody cetuximab to a combination of capecitabine, oxaliplatin, and bevacizumab for metastatic colorectal cancer.
Methods
We randomly assigned 755 patients with previously untreated metastatic colorectal cancer to capecitabine, oxaliplatin, and bevacizumab (CB regimen, 378 patients) or the same regimen plus weekly cetuximab (CBC regimen, 377 patients). The primary end point was progression free survival. The mutation status of the KRAS gene was evaluated as a predictor of outcome.
Results
The median progression free survival was 10.7 months in the CB group and 9.4 in the CBC group (P = 0.01). Quality of life scores were lower in the CBC group. The overall survival and response rates did not differ significantly in the two groups. Treated pat ients in the CBC group had more grade 3 or 4 adverse events, which were at t r ibuted to cetuximab-related adverse cut aneous ef fects. Pat ients t reated with cetuximab who had tumors bearing a mutated KRAS gene had significantly decreased progression-free survival as compared with cetuximab treated patients with wildtype KRAS tumors or patients with mutated KRAS tumors in the CB group.
Conclusions
The addition of cetuximab to capecitabine, oxaliplatin, and bevacizumab resulted in significantly shorter progression-free survival and inferior quality of life. Mutation status of the KRAS gene was a predictor of outcome in the cetuximab group.(ClinicalTrials.gov number, NCT00208546.)
Journals for full download on the link below
We randomly assigned 755 patients with previously untreated metastatic colorectal cancer to capecitabine, oxaliplatin, and bevacizumab (CB regimen, 378 patients) or the same regimen plus weekly cetuximab (CBC regimen, 377 patients). The primary end point was progression free survival. The mutation status of the KRAS gene was evaluated as a predictor of outcome.
Results
The median progression free survival was 10.7 months in the CB group and 9.4 in the CBC group (P = 0.01). Quality of life scores were lower in the CBC group. The overall survival and response rates did not differ significantly in the two groups. Treated pat ients in the CBC group had more grade 3 or 4 adverse events, which were at t r ibuted to cetuximab-related adverse cut aneous ef fects. Pat ients t reated with cetuximab who had tumors bearing a mutated KRAS gene had significantly decreased progression-free survival as compared with cetuximab treated patients with wildtype KRAS tumors or patients with mutated KRAS tumors in the CB group.
Conclusions
The addition of cetuximab to capecitabine, oxaliplatin, and bevacizumab resulted in significantly shorter progression-free survival and inferior quality of life. Mutation status of the KRAS gene was a predictor of outcome in the cetuximab group.(ClinicalTrials.gov number, NCT00208546.)
Journals for full download on the link below
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