Journal Article

<i>STK15</i> polymorphism and breast cancer risk in a population-based study

Kathleen M. Egan, Polly A. Newcomb, Christine B. Ambrosone, Amy Trentham-Dietz, Linda Titus-Ernstoff, John M. Hampton, Makoto T. Kimura and Hiroki Nagase

in Carcinogenesis

Volume 25, issue 11, pages 2149-2153
Published in print November 2004 | ISSN: 0143-3334
Published online November 2004 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgh231
STK15 polymorphism and breast cancer risk in a population-based study

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  • Clinical Cytogenetics and Molecular Genetics

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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.

Keywords: CI, confidence interval; DCIS, ductal carcinoma in situ; OR, odds ratios; SNP, single nucleotide polymorphism

Journal Article.  3574 words. 

Subjects: Clinical Cytogenetics and Molecular Genetics

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