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RIPK1 and CASP7 polymorphism as prognostic markers for survival in patients with colorectal cancer after complete resection

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Abstract

Background

Since apoptosis plays a key role in cancer progression, the present study analyzed the polymorphisms of apoptosis-related genes and their impact on survival after curative resection in patients with colorectal cancer.

Materials and methods

Three hundred and seventy-seven patients were enrolled in the present study. The genomic DNA was extracted from fresh colorectal mucosal tissue, and 15 SNPs of 12 apoptosis-related genes were determined using a Sequenom MassARRAY system.

Results

During the median follow-up of 41.8 (range, 1.1–85.5) months patients alive at last follow-up, 65 relapses and 57 deaths occurred. Among the target polymorphisms, the RIPK1 rs2272990 in a dominant model and the CASP7 rs2227310 in a recessive model of the minor allele were associated with survival in a log-rank test. Moreover, the GA+AA genotype of the RIPK1 rs2272990 and the GG genotype of the CASP7 rs2227310 were significantly correlated with a worse disease-free (hazard ratio [HR] = 2.093; P = 0.007 and HR = 2.641; 0.002, respectively) and disease-specific survival (HR = 2.222; P = 0.013 and HR = 2.247; P = 0.031, respectively) in a multivariate survival analysis.

Conclusion

The RIPK1 and CASP7 polymorphisms can be considered as possible prognostic markers for survival after curative resection in patients with colorectal cancer.

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Conflict of interest statement

All authors certify that we have no financial involvement in any organization or entity with a direct financial interest in the subject matter or materials discussed in this manuscript.

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Correspondence to Jong Gwang Kim or Gyu Seog Choi.

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Chae, Y.S., Kim, J.G., Sohn, S.K. et al. RIPK1 and CASP7 polymorphism as prognostic markers for survival in patients with colorectal cancer after complete resection. J Cancer Res Clin Oncol 137, 705–713 (2011). https://doi.org/10.1007/s00432-010-0929-1

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  • DOI: https://doi.org/10.1007/s00432-010-0929-1

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