Carcinogenesis Advance Access originally published online on July 22, 2004
Carcinogenesis 2004 25(11):2149-2153; doi:10.1093/carcin/bgh231
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Carcinogenesis vol.25 no.11 © Oxford University Press 2004; all rights reserved.
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STK15 polymorphism and breast cancer risk in a population-based study
Vanderbilt University Medical Center, Suite 6000, MCE, Nashville, TN 37232-8300, USA, 1 Cancer Prevention Research Group, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, MP 900, Seattle, WA 98104, USA, 2 Department of Epidemiology, Division of Cancer Prevention and Population Science, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA, 3 Comprehensive Cancer Center and Department of Population Health Sciences, University of Wisconsin, WARF Room 701, 610 Walnut Street, Madison, WI 53726, USA, 4 Dartmouth Medical School, Norris Cotton Cancer Center, Lebanon, NH 03756, USA, 5 University of Wisconsin, WARF Room 307, 610 Walnut Street, Madison, WI 53726, USA, 6 Department of Cancer Genetics, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA
7 To whom correspondence should be addressed. Tel: +1 615 936 1640; Fax: +1 615 936 1269; Email: kathleen.egan{at}vanderbilt.edu
STK15 is considered a potential cancer susceptibility gene owing to its functions in normal cell mitosis. Two common coding region polymorphisms in the gene (F31I and V57I) may affect ubiquitin-dependent degradation and thus the half-life of the encoded protein. There are limited data on the relevance of these polymorphisms to population cancer rates. To examine whether functional variation in STK15 may affect breast cancer risk, we genotyped a large series of incident breast cancer cases (n = 941) and age-matched population controls (n = 830) for the F31I and V57I polymorphisms. Individually, neither the F31I polymorphism [odds ratio (OR) 1.54; 95% confidence interval (CI) 0.96–2.47, comparing 31I with 31F homozygotes] nor the V57I polymorphism (OR 0.92; 95% CI 0.50–1.71, comparing 57I with 57V homozygotes) was significantly associated with breast cancer risk. A relatively common genotype, combining the two polymorphisms (31I-57V/31I-57V, 3% of controls) was related to a significant 2-fold increase in the risk of post-menopausal breast cancer (OR 1.96; 95% CI 1.01–3.79). No interaction was detected between STK15 variants and estrogenic risk factors, although the power of these analyses was limited. These results suggest that STK15 may represent a low penetrance type breast cancer susceptibility gene.
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