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Holt SK, Kwon EM, Lin DW, Ostrander EA, Stanford JL.
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
BACKGROUND: Hepsin (HPN) is one of the most consistently overexpressed genes in prostate cancer and there is some evidence supporting an association between HPN gene variants and prostate cancer risk. We report results from a population-based case-control genetic association study for six tagging single nucleotide polymorphisms (tagSNPs) in the HPN gene. METHODS: Prostate cancer risk was estimated using adjusted unconditional logistic regression in 1,401 incident prostate cancer cases diagnosed in 1993 through 1996 or 2002 through 2005 and 1,351 age-matched controls. Risks of disease recurrence/progression and prostate cancer-specific mortality were estimated using Cox proportional hazards (PH) regression in 437 cases with long-term follow-up. RESULTS: There were 135 recurrence/progression events and 57 cases who died of prostate cancer. Contrary to some earlier studies, we found no evidence of altered risk of developing prostate cancer overall or when clinical measures of tumor aggressiveness were considered for any of the tagSNPs, assessed either individually or by haplotypes. There was no evidence of altered risks of tumor recurrence/progression or prostate cancer death associated with variants in the HPN gene. CONCLUSIONS: Germline genetic variation of HPN does not seem to contribute to risk of prostate cancer or prognosis. Prostate (c) 2010 Wiley-Liss, Inc.
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