title: Genetic variation in RNASEL and risk for prostate cancer in a population-based case-control study.
abstract: BACKGROUND
  Linkage studies have implicated chromosome 1q24 as a putative locus for hereditary prostate cancer. The RNASEL gene maps to 1q24 and has been associated with prostate cancer risk in multiple family-based linkage studies. The RNASEL gene product combats viral infection by degrading viral RNA and inducing apoptosis of infected cells. Few studies have evaluated the role of RNASEL variants in unselected or sporadic prostate cancer, or have considered the potential interaction between RNASEL variants and patient characteristics associated with past infection.
  
  
  METHODS
  Ten SNPs in the RNASEL gene were genotyped in 1,308 prostate cancer cases and 1,267 age-matched controls from prior population-based, case-control studies. The association between each SNP and haplotype with prostate cancer risk was calculated using logistic regression. Associations stratified by Gleason score were evaluated using polytomous regression. The likelihood ratio test was used to investigate effect modification.
  
  
  RESULTS
  Two RNASEL SNPs were associated with overall increases in prostate cancer risk (OR = 1.13 for each variant allele of rs12723593; OR = 1.88 for any variant allele of rs56250729). Risk estimates did not vary substantially by Gleason score, but there was effect modification for the variant allele of rs635261 by history of prostatitis (P = 0.02).
  
  
  CONCLUSIONS
  This study identified three RNASEL variants that are associated with risk for prostate cancer. Further research is required to confirm these results and to better understand the potential role RNASEL variants may play in the etiology of sporadic prostate cancer.
authors.affiliation: Epidemiology Program, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
authors.forename: Megan D
authors.initials: MD
authors.lastname: Fesinmeyer
authors.forename: Erika M
authors.initials: EM
authors.lastname: Kwon
authors.forename: Rong
authors.initials: R
authors.lastname: Fu
authors.forename: Elaine A
authors.initials: EA
authors.lastname: Ostrander
authors.forename: Janet L
authors.initials: JL
authors.lastname: Stanford
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D004722:Endoribonucleases / Q000235:genetics*; D020022:Genetic Predisposition to Disease / Q000453:epidemiology / Q000235:genetics; D014644:Genetic Variation; D006239:Haplotypes; D006801:Humans; D008297:Male; D008875:Middle Aged; D060787:Neoplasm Grading; D020641:Polymorphism, Single Nucleotide; D011471:Prostatic Neoplasms / Q000453:epidemiology / Q000235:genetics / Q000473:pathology; D012307:Risk Factors
chemical_list: D004722:Endoribonucleases; C031956:2-5A-dependent ribonuclease