The Role of Chronic Inflammation in Prostate Carcinogenesis: A Follow-Up Study

Purpose To investigate the role of chronic inflammation in prostatic carcinogenesis with an emphasis on cancers of grade group 2 or above. Methods The presence/absence and extent of chronic inflammation and other relevant pathological findings were assessed using prostate needle biopsies obtained from patients with clinical parameters with suspicion of malignancy. In patients with no prior prostate cancer, follow-up biopsies were reviewed and correlated with the initial pathological findings. Results Of 1,006 prostate needle biopsy cases accessioned over 3 years at our institution, the initial biopsies of 244 cases were identified with no evidence of prostate cancer. These cases were divided into two subsets, including 202 cases with and 42 without chronic inflammation. Pathological findings assessed in this subset included post-atrophic hyperplasia, proliferative inflammatory atrophy, and high-grade prostatic intraepithelial neoplasia (HGPIN). Post-atrophic hyperplasia and proliferative inflammatory atrophy were noted only in patients with chronic inflammation. HGPIN was identified in 22 of the initial biopsy cases, specifically in 21 (10.3%) cases with inflammation and one case (2.4%) without inflammation. In follow-up biopsies, 70 patients (34.7%) with chronic inflammation were found to have prostatic adenocarcinoma with Gleason pattern 3 + 3 (42.9%; grade group 1), Gleason pattern 3 + 4(24.3%; grade group 2), Gleason pattern 4 + 3 (10%; grade group 3) and Gleason scores of 8 or higher (22.8%; grade groups 4 or 5), whereas cancer was found in 10 patients (23.8%) without chronic inflammation in the initial biopsy. Patients whose initial biopsies were benign and without inflammation did not show evidence of high-grade cancer (Gleason score of 8 or higher). Closely encroaching inflammation was observed more frequently in cancers of grade group 2 or above (76.5%, 13/17) compared with grade group 1 (50.0%, 3/6). Conclusions Our findings provide additional data supporting a role for chronic inflammation in the development of prostatic adenocarcinoma.

Duke Scholars

Author Wei Chen Pathology