Strong signature of natural selection within an FHIT intron implicated in prostate cancer risk

PLoS One. 2008;3(10):e3533. doi: 10.1371/journal.pone.0003533. Epub 2008 Oct 27.

Abstract

Previously, a candidate gene linkage approach on brother pairs affected with prostate cancer identified a locus of prostate cancer susceptibility at D3S1234 within the fragile histidine triad gene (FHIT), a tumor suppressor that induces apoptosis. Subsequent association tests on 16 SNPs spanning approximately 381 kb surrounding D3S1234 in Americans of European descent revealed significant evidence of association for a single SNP within intron 5 of FHIT. In the current study, re-sequencing and genotyping within a 28.5 kb region surrounding this SNP further delineated the association with prostate cancer risk to a 15 kb region. Multiple SNPs in sequences under evolutionary constraint within intron 5 of FHIT defined several related haplotypes with an increased risk of prostate cancer in European-Americans. Strong associations were detected for a risk haplotype defined by SNPs 138543, 142413, and 152494 in all cases (Pearson's chi(2) = 12.34, df 1, P = 0.00045) and for the homozygous risk haplotype defined by SNPs 144716, 142413, and 148444 in cases that shared 2 alleles identical by descent with their affected brothers (Pearson's chi(2) = 11.50, df 1, P = 0.00070). In addition to highly conserved sequences encompassing SNPs 148444 and 152413, population studies revealed strong signatures of natural selection for a 1 kb window covering the SNP 144716 in two human populations, the European American (pi = 0.0072, Tajima's D = 3.31, 14 SNPs) and the Japanese (pi = 0.0049, Fay & Wu's H = 8.05, 14 SNPs), as well as in chimpanzees (Fay & Wu's H = 8.62, 12 SNPs). These results strongly support the involvement of the FHIT intronic region in an increased risk of prostate cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Acid Anhydride Hydrolases / genetics*
  • Case-Control Studies
  • DNA Mutational Analysis
  • Gene Expression Profiling
  • Gene Frequency
  • Genetic Predisposition to Disease*
  • Humans
  • Introns*
  • Linkage Disequilibrium
  • Male
  • Neoplasm Proteins / genetics*
  • Polymorphism, Single Nucleotide
  • Prostatic Neoplasms / ethnology
  • Prostatic Neoplasms / genetics*
  • Risk Factors
  • Selection, Genetic*

Substances

  • Neoplasm Proteins
  • fragile histidine triad protein
  • Acid Anhydride Hydrolases