Impact of KRAS Mutation Status on Outcomes in Metastatic Colon Cancer Patients without Anti-Epidermal Growth Factor Receptor Therapy.
- Author:
Seung Tae KIM
1
;
Kyong Hwa PARK
;
Jun Suk KIM
;
Sang Won SHIN
;
Yeul Hong KIM
Author Information
1. Division of Hematology-Oncology, Department of Medicine, Korea University College of Medicine, Seoul, Korea. yhk0215@korea.ac.kr
- Publication Type:Original Article
- Keywords:
KRAS;
Anti-EGFR;
Colorectal neoplasms
- MeSH:
Camptothecin;
Colon;
Colonic Neoplasms;
Colorectal Neoplasms;
Disease-Free Survival;
Endothelial Growth Factors;
Humans;
Multivariate Analysis;
Oncogenes;
Organoplatinum Compounds;
Retrospective Studies
- From:Cancer Research and Treatment
2013;45(1):55-62
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Activating mutation of the KRAS oncogene is an established negative predictor for anti-epidermal growth factor receptor (anti-EGFR) therapies in metastatic colorectal cancer (CRC). However, KRAS mutation as a prognostic factor of survival outcome remains controversial in CRC, independent of anti-EGFR therapies. MATERIALS AND METHODS: We conducted a retrospective analysis of 103 CRC patients who were available for evaluation of KRAS mutation status. None of the patients analyzed had received anti-EGFR therapies. The role of KRAS mutation status was evaluated as a predictive factor for oxaliplatin or irinotecan and as a prognostic factor in CRC patients who did not receive anti-EGFR therapies. RESULTS: Mutations in KRAS were observed in 48.5% of patients. The response for oxaliplatin- (p=0.664) and irinotecan-based (p=0.255) cytotoxic chemotherapy did not differ according to the KRAS mutation status. In addition, no significant difference in progression free survival (PFS; oxaliplatin, p=0.583 and irinotecan, p=0.426) and overall survival (OS; p=0.258) was observed between the wild and mutant type of the KRAS gene. In univariate and multivariate analyses, KRAS mutations did not have a major prognostic value regarding PFS (oxaliplatin: hazard ratio, 0.892; 95% confidence interval [CI], 0.590 to 1.347; p=0.586 and irinotecan: hazard ratio, 0.831; 95% CI, 0.524 to 1.319; p=0.433) or OS (hazard ratio, 0.754; 95% CI, 0.460 to 1.236; p=0.263). In addition, anti-vascular endothelial growth factor therapies did not affect PFS to oxaliplatin or irinotecan and OS. CONCLUSION: KRAS mutation is not a prognostic marker for PFS to oxaliplatin or irinotecan and OS in CRC patients who did not receive anti-EGFR therapies.
