Morphological transition of proliferative inflammatory atrophy to high-grade intraepithelial neoplasia and cancer in human prostate
Article first published online: 8 JUN 2009
Copyright © 2009 Wiley-Liss, Inc.
Volume 69, Issue 13, pages 1378–1386, 15 September 2009
How to Cite
Wang, W., Bergh, A. and Damber, J.-E. (2009), Morphological transition of proliferative inflammatory atrophy to high-grade intraepithelial neoplasia and cancer in human prostate. Prostate, 69: 1378–1386. doi: 10.1002/pros.20992
- Issue published online: 20 AUG 2009
- Article first published online: 8 JUN 2009
- Manuscript Accepted: 4 MAY 2009
- Manuscript Received: 2 MAR 2009
- Swedish Cancer Society
- Sahlgrenska University Hospital
- af Jochnick Foundation
- Swedish Medical Society
- Swedish Johanniterhjälpen
- Research Foundations of C. & S. Hagströmers
- A. Gabrielssons, M. & B. Gustavssons, P. Falks, G. Nilssons, and M. Bergvalls
- proliferative inflammatory atrophy;
- prostate cancer
Inflammation has been implicated as a potential etiological agent in human prostate cancer (PCa). Proliferative inflammatory atrophy (PIA) in prostate consists of areas of glandular atrophy associated with chronic inflammation and epithelial cell proliferation. It has been suggested that PIA is a candidate precursor of prostate malignancy. We aimed to explore the morphological transition between PIA and co-existing high-grade prostate intraepithelial neoplasia (HGPIN) and/or PCa.
Serial slides of 50 whole-mounted radical prostatectomies were studied with H&E staining and immunostaining of cytokeratin 5 (CK5), glutathione S-transferase pi (GSTP1), hepatocyte growth factor receptor (c-MET), CCAAT/enhancer binding protein β (C/EBPβ), and Ki-67. Utilizing immunohistochemical stains to examine HGPIN, PIA-merging HGPIN, and PIA-merging PCa lesions, respectively.
A total of 1,188 HGPIN lesions were identified, of which 17% (198) were in the morphological process of merging with PIA. Thirty-six PIA-merging PCa lesions were also detected. The atrophic epithelial cells in such merging lesions had increased Ki-67 index and an intermediate phenotype: increased expression for CK5, GSTP1, c-MET, and C/EBPβ. In addition, clusters of atypical epithelial cell hyperplasia, that is, with nuclear enlargement, hyperchromasia, and prominent nucleoli, were found in 16 PIA lesions. Such clusters of atypical cells that meet the criteria for HGPIN still expressed CK5 and were adjacent to focal chronic inflammation.
Direct morphological transition between PIA and HGPIN and/or PCa was present. The atrophic cells in these merging lesions had an intermediate phenotype. Clusters of atypical epithelial cell hyperplasia might represent the earliest transition from PIA to HGPIN. Prostate 69: 1378–1386, 2009. © 2009 Wiley-Liss, Inc.