Molecular evidence supporting the precursor nature of atypical adenomatous hyperplasia of the prostate. Issue 7 (28th March 2019)

• Record Type: Journal Article
• Authors: Cheng, Liang; Montironi, Rodolfo; Davidson, Darrell D.; Wang, Mingsheng; Lopez‐Beltran, Antonio; Zhang, Shaobo
• Is Part Of: Molecular carcinogenesis. Volume 58:Issue 7(2019)
• Page Start: 1272
• Page End: 1278
• Publication Date: 2019-03-28
• Subjects: atypical adenomatous hyperplasia -- carcinogenesis -- high‐grade prostatic intraepithelial neoplasia -- precursor/premalignant lesions -- prostate -- telomere; Carcinogenesis -- Molecular aspects -- Periodicals; 616.994071
• DOI: 10.1002/mc.23009
• Languages: English
• ISSNs: 0899-1987

Abstract

Abstract: Atypical adenomatous hyperplasia (AAH) of the prostate is characterized by lobular proliferation of closely packed small acini. It is hypothesized that AAH is a precursor lesion for low‐grade prostate cancer arising from the transition zone. Telomere dysfunction is common during malignant transformation of epithelia. In this study, we investigate telomere shortening in AAH ( n = 93), high‐grade prostatic intraepithelial neoplasia (HGPIN) ( n = 68), and prostatic adenocarcinoma (PCA) ( n = 70) using quantitative fluorescence in situ hybridization. Twenty percent (19 of 93) of AAH specimens, 68% (46 of 68) of HGPIN, and 83% (58 of 70) of PCA showed significant telomere shortening. Thirty‐two percent of AAH lesions had α‐methylacyl‐CoA racemase (AMACR) expression, a sensitive and specific marker for HGPIN and PCA. AMACR expression in AAH was seen more frequently in AAH foci with telomere shortening or coexisting PCA. Our findings indicate that a subset of AAH lesions have telomere shortening and AMACR expression, suggesting that these foci may be precursors for PCA.