¹Section of Cancer Genetics, Institute of Cancer Research, Surrey, UK

Correspondence: Professor RS Houlston, Section of Cancer Genetics, Brookes Lawley Building, Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK. E-mail: Richard.Houlston@icr.ac.uk

Received 20 June 2006; Revised 29 August 2006; Accepted 29 August 2006; Published online 26 September 2006.

Abstract

Recently, homozygosity for T91A single-nucleotide polymorphism (SNP) in the serine/threonine kinase (STK15) gene, which generates the substitution F31I has been proposed to increase the risk of a number of tumours including colorectal cancer (CRC). To further evaluate the relationship between STK15 F31I and risk of CRC, we genotyped 2558 CRC cases and 2680 controls for this polymorphism. We found no evidence that homozygosity for the STK15 31I genotype confers an increased risk of CRC (odds ratio=0.95, 95% confidence interval (CI): 0.74–1.24). We also conducted a kin-cohort analysis to assess risk among first-degree relatives of the CRC cases. The hazard ratio for I/I homozygotes compared to F/F homozygotes was 1.65 (95% CI: 0.39–3.17). A meta-analysis of our case–control data and three previous studies also provided no evidence of an elevated risk of CRC associated with homozygosity. These data provide no support for the hypothesis that sequence variation in STK15 defined by SNP F31I per se confers an elevated risk of CRC.