title: Postatrophic hyperplasia of the prostate in Japan: histologic and immunohistochemical features and p53 gene mutation analysis.
abstract: BACKGROUND
  Postatrophic hyperplasia (PAH) is one of the patterns of prostatic atrophy but has been regarded as a precursor of prostatic cancer (PCA) because of its possible increase in proliferative activity compared with simple atrophy and morphologic mimicry of PCA.
  
  
  METHODS
  Radical prostatectomy specimens obtained from 28 patients with PCA were analyzed by histologic and immunohistochemical methods by using 34 beta E12 and Ki-67 as primary antibodies. Tissue from PAH, PCA, high-grade prostatic intraepithelial neoplasia (HGPIN), a possible precursor of PCA, and benign hyperplasia were microdissected and p53 gene mutations were examined by the polymerase chain reaction-single strand conformation polymorphism method followed by direct sequencing.
  
  
  RESULTS
  Histologically, PAH consists of compactly arranged small acini with irregular atrophic-appearing contours, mimicking PCA. PAH lesions were detected in 7 (25%) of 28 cases with PCA: multifocal in 6 of 7 (85.7%) cases, maximum size of lesions ranged from 0.3 to 2.3 mm. Mild nuclear enlargement and small nucleoli were observed in all cases. Capsular or perineural invasion, crystalloids, and mitotic figures were not found in any case. Inflammatory changes and fibrosis near PAH were found in 100% and 71% of cases, respectively. PAH involved non-transition zone in all cases and occasionally involved transition zone. Forty-three percent of PAH lesions were in proximity (<2 mm) to PCA. None of the clinical and pathologic factors examined were correlated with the presence of PAH. Immunohistochemical analysis by using 34 beta E12 revealed intact basal cells. Proliferative activity defined by positive rate for labeling with MIB-1 antibody was intermediate between benign prostatic hyperplasia and HGPIN. The frequency of p53 mutations in PAH lesions was 5.3%, which was similar to that in HGPIN lesions (4.2%). Benign glands never showed mutations.
  
  
  CONCLUSIONS
  These findings suggested that PAH might be a precursor for PCA.
authors.affiliation: Department of Pathology, Osaka University Medical School, Suita, Osaka, Japan.
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Tsujimoto
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Takayama
authors.forename: Norio
authors.initials: N
authors.lastname: Nonomura
authors.forename: Akihiko
authors.initials: A
authors.lastname: Okuyama
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Aozasa
mesh_terms: D000368:Aged; D002455:Cell Division; D004252:DNA Mutational Analysis; D005355:Fibrosis; D016158:Genes, p53 / Q000235:genetics*; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation; D007564:Japan; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D011230:Precancerous Conditions; D011468:Prostatectomy; D011470:Prostatic Hyperplasia / Q000208:ethnology / Q000235:genetics* / Q000276:immunology; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000503:physiopathology