title: Clinical and pathologic significance of activation of signal transducer and activator of transcription 3 in prostate cancer.
abstract: OBJECTIVE
  To evaluate the association of signal transducer and activator of transcription 3 (STAT3) with the invasiveness and aggressiveness of localized prostate cancer.
  
  
  METHODS
  Paraffin-embedded specimens from 92 patients with clinically localized prostate cancer who underwent radical prostatectomy without neoadjuvant treatment were analyzed by immunohistochemistry using two antibodies: anti-phospho-specific STAT3 (p-STAT3) antibody, which recognized only activated STAT3, and anti-total STAT3 antibody, which recognized both activated and inactivated STAT3. The patients were separated into one of four groups according to the percentage of the cells with positive nuclear staining using a 0 to 3+ scoring system. The associations between the immunostaining and invasiveness and aggressiveness of clinically localized prostate cancer were analyzed.
  
  
  RESULTS
  Pathologically, 66 patients (71.7%) had organ-confined disease. Of the 92 tumors examined, 8, 20, 23, and 41 showed staining patterns for p-STAT3 of 0, 1+, 2+, and 3+, respectively. In addition, 0, 3, 2, and 87 tumors showed staining patterns for STAT3 of 0, 1+, 2+, and 3+, respectively. The staining patterns for p-STAT3 correlated significantly with pathologic stage, Gleason score, and extracapsular extension. No significant correlation was found between p-STAT3 immunostaining and microvascular invasion, perineural invasion, or seminal vesicle invasion. Patients with 3+ immunostaining of p-STAT3 had a significantly greater biochemical prostate-specific antigen failure rate than those with 2+ or less immunostaining.
  
  
  CONCLUSIONS
  Increased p-STAT3 immunoreactivity showed a highly invasive and aggressive potential in patients with localized prostate cancer treated with radical prostatectomy. This suggests that STAT3 signaling contributes to the invasiveness and aggressiveness of prostate cancer.
authors.affiliation: Department of Urology, Keio University School of Medicine, Tokyo, Japan. m5508985@ra2.so-net.ne.jp
authors.forename: Minoru
authors.initials: M
authors.lastname: Horinaga
authors.forename: Hajime
authors.initials: H
authors.lastname: Okita
authors.forename: Jun
authors.initials: J
authors.lastname: Nakashima
authors.forename: Kent
authors.initials: K
authors.lastname: Kanao
authors.forename: Michiie
authors.initials: M
authors.lastname: Sakamoto
authors.forename: Masaru
authors.initials: M
authors.lastname: Murai
mesh_terms: D000368:Aged; D006801:Humans; D008297:Male; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D011471:Prostatic Neoplasms / Q000737:chemistry* / Q000235:genetics / Q000473:pathology*; D050796:STAT3 Transcription Factor / Q000032:analysis* / Q000235:genetics
chemical_list: D050796:STAT3 Transcription Factor