title: Immunohistochemical expression of retinoblastoma and p53 tumor suppressor genes in prostatic intraepithelial neoplasia: comparison with prostatic adenocarcinoma and benign prostate.
abstract: Mutational alterations involving the p53 and retinoblastoma (RB) tumor suppressor genes are implicated in the oncogenesis of a variety of tumors. Their role in the pathogenesis of prostatic adenocarcinoma remains to be fully elucidated, and their detection in high-grade prostatic intraepithelial neoplasia (HG-PIN) has not been closely examined. We studied the immunohistochemical expression of RB and p53 proteins in HG-PIN, benign prostate, and prostatic adenocarcinoma from 25 radical prostatectomy specimens. Formalin-fixed, paraffin-embedded tissue sections pretreated with antigen retrieval in citrate buffer were stained with anti-RB antibody RB-WL-1 and anti-p53 antibody DO-7. RB immunoreactivity was present in all of the cases in the foci of HG-PIN, benign prostate, and prostatic adenocarcinoma. Mutant p53 protein was detected in 56% of HG-PIN, 72% of prostatic adenocarcinomas, and 20% of benign prostatic glands. A multivariate analysis of variance showed an overall difference in p53 immunoreactivity between HG-PIN, benign prostate, and prostatic adenocarcinoma (P < .001). There was a statistically significant difference between immunoreactivity of the benign prostate and of HG-PIN (P < .001) and between the immunoreactivity of benign prostate and prostatic adenocarcinoma (P < .001). The immunoreactivities of HG-PIN and prostatic adenocarcinoma were not statistically different (P = .3). These data suggest that RB loss might not play a role in initiation of all cases of prostatic adenocarcinoma. The p53 immunoreactivity in HG-PIN was significantly different from that found in benign prostate and was similar to that of prostatic adenocarcinoma. This is in keeping with the putative premalignant character of HG-PIN.
authors.affiliation: Department of Pathology, Henry Ford Hospital, Detroit, Michigan 48202, USA.
authors.forename: P
authors.initials: P
authors.lastname: Tamboli
authors.forename: M B
authors.initials: MB
authors.lastname: Amin
authors.forename: H J
authors.initials: HJ
authors.lastname: Xu
authors.forename: M D
authors.initials: MD
authors.lastname: Linden
mesh_terms: D000230:Adenocarcinoma / Q000737:chemistry / Q000473:pathology; D014408:Biomarkers, Tumor / Q000032:analysis / Q000096:biosynthesis; D015870:Gene Expression; D016161:Genes, Retinoblastoma / Q000235:genetics*; D016158:Genes, p53 / Q000235:genetics*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D009367:Neoplasm Staging; D011467:Prostate / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D011470:Prostatic Hyperplasia / Q000473:pathology; D019048:Prostatic Intraepithelial Neoplasia / Q000737:chemistry* / Q000235:genetics* / Q000473:pathology; D011471:Prostatic Neoplasms / Q000737:chemistry / Q000235:genetics* / Q000473:pathology; D016160:Retinoblastoma Protein / Q000032:analysis; D012189:Retrospective Studies; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: D014408:Biomarkers, Tumor; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53