Polymorphisms in the FGF2 Gene and Risk of Serous Ovarian Cancer: Results From the Ovarian Cancer Association Consortium

Fibroblast growth factor (FGF)-2 (basic) is a potent angiogenic molecule involved in tumor progression, and is one of several growth factors with a central role in ovarian carcinogenesis. We hypothesized that common single nucleotide polymorphisms (SNPs) in the FGF2 gene may alter angiogenic potenti...

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Published inTwin research and human genetics Vol. 12; no. 3; pp. 269 - 275
Main Authors Johnatty, Sharon E., Beesley, Jonathan, Chen, Xiaoqing, Spurdle, Amanda B., DeFazio, Anna, Webb, Penelope M., Goode, Ellen L., Rider, David N., Vierkant, Robert A., Anderson, Stephanie, Wu, Anna H., Pike, Malcolm, Van Den Berg, David, Moysich, Kirsten, Ness, Roberta, Doherty, Jennifer, Rossing, Mary-Anne, Pearce, Celeste Leigh, Chenevix-Trench, Georgia
Format Journal Article
LanguageEnglish
Published Cambridge, UK Cambridge University Press 01.06.2009
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Summary:Fibroblast growth factor (FGF)-2 (basic) is a potent angiogenic molecule involved in tumor progression, and is one of several growth factors with a central role in ovarian carcinogenesis. We hypothesized that common single nucleotide polymorphisms (SNPs) in the FGF2 gene may alter angiogenic potential and thereby susceptibility to ovarian cancer. We analyzed 25 FGF2 tgSNPs using five independent study populations from the United States and Australia. Analysis was restricted to non-Hispanic White women with serous ovarian carcinoma (1269 cases and 2829 controls). There were no statistically significant associations between any FGF2 SNPs and ovarian cancer risk. There were two nominally statistically significant associations between heterozygosity for two FGF2 SNPs (rs308379 and rs308447; p < .05) and serous ovarian cancer risk in the combined dataset, but rare homozygous estimates did not achieve statistical significance, nor were they consistent with the log additive model of inheritance. Overall genetic variation in FGF2 does not appear to play a role in susceptibility to ovarian cancer.
Bibliography:ark:/67375/6GQ-9K27HFX8-S
PII:S1832427400009853
Address for correspondence: G. Chenevix-Trench, Cancer and Cell Biology, Queensland Institute of Medical Research, c/o Royal Brisbane Hospital Post Office, Herston, QLD 4029, Australia.
istex:8F0D65A3B3E8FC140F96032CB7979CCA1E661803
ArticleID:00985
Twin Research and Human Genetics, Vol. 12, No. 3, June 2009: 269-275
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ISSN:1832-4274
1839-2628
DOI:10.1375/twin.12.3.269