title: Molecular profiling of benign prostatic hyperplasia using a large scale real-time reverse transcriptase-polymerase chain reaction approach.
abstract: OBJECTIVE
  Benign prostatic hyperplasia (BPH) is characterized by a hyperplastic growth of epithelial and stromal cells in the prostate. Despite the high prevalence of the disease little is known regarding the molecular etiology of BPH. Therefore, a comparison of gene expression patterns between normal prostate, BPH and prostate cancer could provide insights into the pathogenic mechanisms of the disease and identify candidate genes that could be targeted for therapeutic use.
  
  
  METHODS
  Prostate tissue specimen were obtained from 30 patients undergoing adenomectomy for BPH. Adenoma weight was less than 60 gm in 15 patients and more than 60 gm in the remainder. Normal prostate tissue was obtained from 15 patients undergoing radical prostatectomy for cancer from areas selected for absent tumor and BPH. Two pools of organ confined prostate cancer were also analyzed. We quantified in the 5 pools of tissues the expression of 327 genes using real-time quantitative reverse transcriptase-polymerase chain reaction.
  
  
  RESULTS
  A total of 23 genes showed increased expression in BPH with a fold change of at least 2.5 between normal prostate and the 2 BPH groups, of which most were normal or down-regulated in prostate cancer. Seven genes showed decreased expression in BPH with a fold change of at least 3.5 between normal prostate and BPH. Most of them were also normal or down-regulated in prostate cancer.
  
  
  CONCLUSIONS
  We identified a set of genes up-regulated in BPH compared to normal prostate tissue and often prostate cancer, including genes previously implicated in BPH and others not previously linked to this disease to our knowledge. Further investigations are now warranted to determine the clinical relevance and therapeutic potential of these genes.
authors.affiliation: CeRePP-EA 3104, Universite Paris 7 (UFR Biomédicale), Paris, France.
authors.forename: Gaëlle
authors.initials: G
authors.lastname: Fromont
authors.forename: Laurent
authors.initials: L
authors.lastname: Chene
authors.forename: Alain
authors.initials: A
authors.lastname: Latil
authors.forename: Ivan
authors.initials: I
authors.lastname: Bieche
authors.forename: Michel
authors.initials: M
authors.lastname: Vidaud
authors.forename: Guy
authors.initials: G
authors.lastname: Vallancien
authors.forename: Philippe
authors.initials: P
authors.lastname: Mangin
authors.forename: Georges
authors.initials: G
authors.lastname: Fournier
authors.forename: Pierre
authors.initials: P
authors.lastname: Validire
authors.forename: Olivier
authors.initials: O
authors.lastname: Cussenot
mesh_terms: D000368:Aged; D002455:Cell Division / Q000235:genetics*; D004847:Epithelial Cells / Q000473:pathology; D005347:Fibroblasts / Q000473:pathology; D015870:Gene Expression / Q000502:physiology; D020869:Gene Expression Profiling; D006133:Growth Substances / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D011467:Prostate / Q000473:pathology; D011470:Prostatic Hyperplasia / Q000235:genetics* / Q000473:pathology; D012016:Reference Values; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods*; D017154:Stromal Cells / Q000473:pathology; D015854:Up-Regulation / Q000502:physiology
chemical_list: D006133:Growth Substances