ArticlePloS one2008
Strong signature of natural selection within an FHIT intron implicated in prostate cancer risk.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Divergent evolution of hepatocellular carcinoma genomes in chimpanzees and humans.Evolution, medicine, and public health · 2026Article
- Evolutionary selection of alleles in the melanophilin gene that impacts on prostate organ function and cancer risk.Evolution, medicine, and public health · 2021Article
- DNA polymorphism and selection at the bindin locus in three Strongylocentrotus sp. (Echinoidea).BMC genetics · 2016Article
- Common Variants Affecting Susceptibility to Develop Multiple Basal Cell Carcinomas.The Journal of investigative dermatology · 2015Article
- Computational Survey of FHIT, A Putative Human Tumor Suppressor, Truncates Structure.Avicenna journal of medical biotechnology · 2014Article
- Evolutionary molecular medicine.Journal of molecular medicine (Berlin, Germany) · 2012Review
- Single nucleotide polymorphisms of Toll-like receptor 4 decrease the risk of development of hepatocellular carcinoma.PloS one · 2011Article
- The emergence of human-evolutionary medical genomics.Evolutionary applications · 2011Article
- Allelic imbalance and abnormal expression of FHIT in endemic nasopharyngeal carcinoma: association with clinicopathological features.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2010Article
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Authors and funding
18 authors at 12 institutions in 1 country.
Funding
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.
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