NDLI: Association between invasive ovarian cancer susceptibility and 11 best candidate SNPs from breast cancer genome-wide association study

Content Provider	PubMed Central
Author	Song, Honglin Ramus, Susan J. Kjaer, Susanne Krüger Dicioccio, Richard A. Chenevix Trench, Georgia Pearce, Celeste Leigh Hogdall, Estrid Whittemore, Alice S. Mcguire, Valerie Claus, Hogdall Jan, Blaakaer Wu, Anna H. Berg, David J. Van Den Stram, Daniel O. Menon, Usha Gentry-maharaj, Aleksandra Jacobs, Ian J. Webb, Penny M. Beesley, Jonathan Chen, Xiaoqing Rossing, Mary Anne Doherty, Jennifer A. Jenny, Chang-claude Shan, Wang-gohrke Goodman, Marc T. Lurie, Galina Thompson, Pamela J. Carney, Michael E. Ness, Roberta B. Kirsten, Moysich Goode, Ellen L. Vierkant, Robert A. Cunningham, Julie M. Anderson, Stephanie Schildkraut, Joellen M. Andrew, Berchuck Iversen, Edwin S. Moorman, Patricia G. Montserrat, Garcia-closas Chanock, Stephen Lissowska, Jolanta Brinton, Louise Hoda, Anton-culver Ziogas, Argyrios Brewster, Wendy R. Ponder, Bruce A. J. Easton, Douglas F. Gayther, Simon A. Pharoah, Paul D. P.
Abstract	Because both ovarian and breast cancer are hormone-related and are known to have some predisposition genes in common, we evaluated 11 of the most significant hits (six with confirmed associations with breast cancer) from the breast cancer genome-wide association study for association with invasive ovarian cancer. Eleven SNPs were initially genotyped in 2927 invasive ovarian cancer cases and 4143 controls from six ovarian cancer case–control studies. Genotype frequencies in cases and controls were compared using a likelihood ratio test in a logistic regression model stratified by study. Initially, three SNPs (rs2107425 in MRPL23, rs7313833 in PTHLH, rs3803662 in TNRC9) were weakly associated with ovarian cancer risk and one SNP (rs4954956 in NXPH2) was associated with serous ovarian cancer in non-Hispanic white subjects (P-trend < 0.1). These four SNPs were then genotyped in an additional 4060 cases and 6308 controls from eight independent studies. Only rs4954956 was significantly associated with ovarian cancer risk both in the replication study and in combined analyses. This association was stronger for the serous histological subtype [per minor allele odds ratio (OR) 1.07 95% CI 1.01–1.13, P-trend = 0.02 for all types of ovarian cancer and OR 1.14 95% CI 1.07–1.22, P-trend = 0.00017 for serous ovarian cancer]. In conclusion, we found that rs4954956 was associated with increased ovarian cancer risk, particularly for serous ovarian cancer. However, none of the six confirmed breast cancer susceptibility variants we tested was associated with ovarian cancer risk. Further work will be needed to identify the causal variant associated with rs4954956 or elucidate its function.
Related Links	http://dx.doi.org/10.1093/hmg/ddp138
Ending Page	2304
Page Count	8
Starting Page	2297
File Format	PDF
ISSN	09646906
e-ISSN	14602083
Journal	Human Molecular Genetics
Issue Number	12
Volume Number	18
Language	English
Publisher	Oxford University Press
Publisher Date	2009-06-15
Access Restriction	Open
Rights Holder	Oxford University Press
Subject Keyword	Genetics(clinical) Genetics Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Genetics Molecular Biology Genetics (clinical)

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