Dose KRAS Mutation Status Affect on the Effect of VEGF Therapy in Metastatic Colon Cancer Patients?
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PurposeMutations affecting the KRAS gene are an established negative predictor for antiepidermalgrowth factor receptor (anti-EGFR) therapies in metastatic colorectal cancer(CRC). However, the role of KRAS mutation as a biomarker for anti-vascular endothelialgrowth factor (VEGF) remains controversial. Materials and MethodsWe analyzed retrospective data from 32 CRC patients who were available for KRASmutation status and received cytotoxic chemotherapy plus bevacizumab as a first-linetherapy. Six of 32 patients received anti-EGFR therapies. We used KRAS mutationstatus as a predictive or prognostic factor in CRC patients receiving bevacizumab. ResultsWe observed mutations in KRAS in 59.4% of patients. Bevacizumab was used incombination with oxaliplatin based regimens. There was no significant difference forprogression free survival (PFS) and overall survival (OS) in patients with oxaliplatinbased cytotoxic chemotherapy plus bevacizumab according to the status of KRASmutation. After first-line therapy, 28 patients (87.5%) received second-line therapy. In univariate analysis, KRAS mutations did not have a major prognostic value for PFS(hazard ratio, 1.007; 95% confidence interval [CI], 0.469 to 2.162; p＞0.05) or OS(hazard ratio, 0.548; 95% CI, 0.226 to 1.328; p＞0.05). In addition, anti-EGFRtherapies did not affect the impact on OS. ConclusionKRAS mutation is neither a predictive for bevacizumab nor a prognostic for OS in CRCpatients receiving anti-VEGF therapy.
Abstract
PurposeMutations affecting the KRAS gene are an established negative predictor for antiepidermalgrowth factor receptor (anti-EGFR) therapies in metastatic colorectal cancer(CRC). However, the role of KRAS mutation as a biomarker for anti-vascular endothelialgrowth factor (VEGF) remains controversial. Materials and MethodsWe analyzed retrospective data from 32 CRC patients who were available for KRASmutation status and received cytotoxic chemotherapy plus bevacizumab as a first-linetherapy. Six of 32 patients received anti-EGFR therapies. We used KRAS mutationstatus as a predictive or prognostic factor in CRC patients receiving bevacizumab. ResultsWe observed mutations in KRAS in 59.4% of patients. Bevacizumab was used incombination with oxaliplatin based regimens. There was no significant difference forprogression free survival (PFS) and overall survival (OS) in patients with oxaliplatinbased cytotoxic chemotherapy plus bevacizumab according to the status of KRASmutation. After first-line therapy, 28 patients (87.5%) received second-line therapy. In univariate analysis, KRAS mutations did not have a major prognostic value for PFS(hazard ratio, 1.007; 95% confidence interval [CI], 0.469 to 2.162; p＞0.05) or OS(hazard ratio, 0.548; 95% CI, 0.226 to 1.328; p＞0.05). In addition, anti-EGFRtherapies did not affect the impact on OS. ConclusionKRAS mutation is neither a predictive for bevacizumab nor a prognostic for OS in CRCpatients receiving anti-VEGF therapy.
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