title: Increased CD59 protein expression predicts a PSA relapse in patients after radical prostatectomy.
abstract: BACKGROUND
  Human protectin (CD59) is a regulator of complement activation that inhibits complement-mediated cell lysis, and thus might confer immune resistance to tumor cells. CD59 expression has been described in a variety of human malignancies, including breast cancer. Since a comprehensive investigation of CD59 expression in prostate cancer has not been conducted yet, we aimed to determine the significance of CD59 expression in prostate cancer.
  
  
  METHODS
  Eighty-six primary adenocarcinomas of the prostate were immunostained using a monoclonal CD59 antibody (clone MEM-43) and a standard detection system. The immunoreactivity of the tumor was evaluated as low versus high for statistical analysis. Additionally, CD59 mRNA levels were determined by real-time PCR in matched (tumor/normal) microdissected tissues from 26 cases.
  
  
  RESULTS
  Cytoplasmic CD59 immunoreactivity was found in epithelia of prostate cancer, prostatic intraepithelial neoplasia, benign hyperplasia, atrophic, and normal glands. High rates of CD59 expression were noted in 36% of prostate cancer cases and were significantly associated with tumor pT stage (P = 0.043), Gleason grade (P = 0.013) and earlier biochemical (PSA) relapse in Kaplan-Meier analysis (P = 0.0013). On RNA level, we found an upregulation in 19.2% (five cases), although the general rate of CD59 transcript was significantly lower in tumor tissue (P = 0.03).
  
  
  CONCLUSIONS
  CD59 protein is strongly expressed in 36% of adenocarcinomas of the prostate and and is associated with disease progression and adverse patient prognosis.
authors.affiliation: Department of Urology, Charité University Hospital, Berlin, Germany.
authors.forename: Chuanliang
authors.initials: C
authors.lastname: Xu
authors.forename: Monika
authors.initials: M
authors.lastname: Jung
authors.forename: Mick
authors.initials: M
authors.lastname: Burkhardt
authors.forename: Carsten
authors.initials: C
authors.lastname: Stephan
authors.forename: Dietmar
authors.initials: D
authors.lastname: Schnorr
authors.forename: Stefan
authors.initials: S
authors.lastname: Loening
authors.forename: Klaus
authors.initials: K
authors.lastname: Jung
authors.forename: Manfred
authors.initials: M
authors.lastname: Dietel
authors.forename: Glen
authors.initials: G
authors.lastname: Kristiansen
mesh_terms: D000230:Adenocarcinoma / Q000276:immunology* / Q000473:pathology / Q000601:surgery; D000368:Aged; D018957:CD59 Antigens / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D015331:Cohort Studies; D018450:Disease Progression; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009364:Neoplasm Recurrence, Local / Q000276:immunology* / Q000473:pathology; D017430:Prostate-Specific Antigen / Q000097:blood*; D011468:Prostatectomy; D011471:Prostatic Neoplasms / Q000276:immunology* / Q000473:pathology / Q000601:surgery; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D012189:Retrospective Studies; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016019:Survival Analysis
chemical_list: D018957:CD59 Antigens; D012333:RNA, Messenger; D017430:Prostate-Specific Antigen