title: Gene polymorphisms and prostate cancer: the evidence.
abstract: OBJECTIVE
  Prostate cancer is still the most frequent noncutaneous male malignancy and is the second most common cause of cancer death. Genetic factors have been extensively studied in different countries. In addition, numerous genome-wide association studies have been performed in developed countries. Genetic tests will be applied in the near future for diagnosis, therapeutic, and prognostic significance. Therefore, we reviewed the association of several important pathways and genes with critical functions in prostate cancer development or progression.
  
  
  METHODS
  We performed a PubMed search using several key words such as prostate cancer, names of important genes with critical function, and polymorphisms. Then, we reviewed retrieved articles as well as relevant articles from 1997 to 2009.
  
  
  RESULTS
  There are conflicting results of studies on some gene polymorphisms in association with prostate cancer. Most of the inconsistent results have been reported in studies investigating the vitamin D receptor gene polymorphism in association with prostate cancer. Genes related to angiogenesis and cell adhesion genes are more promising. Following results of future studies, the use of antibodies blocking over-expressed genes or proteins may be supported in patients with prostate cancer.
  
  
  CONCLUSIONS
  The difference between the results of studies on gene polymorphisms in prostate cancer may be explained partly by ethnic differences, limited sample size, and other risk or protective factors modifying these effects. Genome-wide studies are currently performed in developed countries and extensive use of this type of analysis may merit consideration in other countries. Furthermore, future studies are needed to further investigate environmental and diet factors interactions with genetic factors.
authors.affiliation: Department of Urology, School of Medicine, New York University, NY, USA.
authors.forename: Seyed S
authors.initials: SS
authors.lastname: Dianat
authors.forename: Markus
authors.initials: M
authors.lastname: Margreiter
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Eckersberger
authors.forename: Julia
authors.initials: J
authors.lastname: Finkelstein
authors.forename: Franklin
authors.initials: F
authors.lastname: Kuehas
authors.forename: Ralf
authors.initials: R
authors.lastname: Herwig
authors.forename: Mohsen
authors.initials: M
authors.lastname: Ayati
authors.forename: Herbert
authors.initials: H
authors.lastname: Lepor
authors.forename: Bob
authors.initials: B
authors.lastname: Djavan
mesh_terms: D002448:Cell Adhesion / Q000235:genetics; D018816:Genes, cdc; D056426:Genetic Loci / Q000235:genetics; D020022:Genetic Predisposition to Disease; D055106:Genome-Wide Association Study; D006801:Humans; D008297:Male; D009389:Neovascularization, Pathologic / Q000235:genetics; D011110:Polymorphism, Genetic / Q000235:genetics*; D011471:Prostatic Neoplasms / Q000235:genetics*; D018167:Receptors, Calcitriol / Q000235:genetics; D012307:Risk Factors
chemical_list: D018167:Receptors, Calcitriol