Common variation in the fibroblast growth factor receptor 2 gene is not associated with endometriosis risk

Hum Reprod. 2008 Jul;23(7):1661-8. doi: 10.1093/humrep/den035. Epub 2008 Feb 18.

Abstract

Background: Endometriosis is a polygenic disease with a complex and multifactorial aetiology that affects 8-10% of women of reproductive age. Epidemiological data support a link between endometriosis and cancers of the reproductive tract. Fibroblast growth factor receptor 2 (FGFR2) has recently been implicated in both endometrial and breast cancer. Our previous studies on endometriosis identified significant linkage to a novel susceptibility locus on chromosome 10q26 and the FGFR2 gene maps within this linkage region. We therefore hypothesized that variation in FGFR2 may contribute to the risk of endometriosis.

Methods: We genotyped 13 single nucleotide polymorphisms (SNPs) densely covering a 27 kb region within intron 2 of FGFR2 including two SNPs (rs2981582 and rs1219648) significantly associated with breast cancer and a total 40 tagSNPs across 150 kb of the FGFR2 gene. SNPs were genotyped in 958 endometriosis cases and 959 unrelated controls.

Results: We found no evidence for association between endometriosis and FGFR2 intron 2 SNPs or SNP haplotypes and no evidence for association between endometriosis and variation across the FGFR2 gene.

Conclusions: Common variation in the breast-cancer implicated intron 2 and other highly plausible causative candidate regions of FGFR2 do not appear to be a major contributor to endometriosis susceptibility in our large Australian sample.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Endometriosis / genetics*
  • Female
  • Genetic Variation*
  • Humans
  • Linkage Disequilibrium
  • Polymorphism, Single Nucleotide
  • Receptor, Fibroblast Growth Factor, Type 2 / genetics*
  • Risk

Substances

  • FGFR2 protein, human
  • Receptor, Fibroblast Growth Factor, Type 2