Does smoking change expression patterns of the tumor suppressor and DNA repair genes in the prostate gland?

Objectives: Somatic mutations can be present in clonally expanded cell populations in nonmalignant tissues, which are detectable at tissue-level resolution. Some of the mutational changes may arise due to smoking. We aimed to find out changes in carcinogenic gene expressions related to smoking in nonmalignant prostate gland epithelia.

Materials And Methods: The patients who came to the Department of Urology at Abant Izzet Baysal University Medical Faculty from December 2006 to December 2009 for prostate biopsy were questioned for cigarette smoking. The patients were divided into 2 groups, namely, smokers and nonsmokers. Paraffin sections were stained immunohistochemically with p53, PTEN, p16INK4a, MSH2, CHK2, RB, and E-cadherin.

Results: Smoking was the main independent factor that had an effect on the immunohistochemical expressions for p53, p16, and PTEN (P = 0.007, P = 0.036, P = 0.015, respectively). Age and inflammation had no statistically significant effects on gene expressions. No difference was found between smokers and nonsmokers for immunohistochemical expressions of E-cadherin, MSH2, RB, and CHK2.

Conclusions: Smoking-related carcinogens can alter the expressions of some suppressor genes in a prostate tissue, and these alterations can be determined immunohistochemically. Alterations in these genes in prostate gland epithelia could possibly increase the risk for prostate carcinoma.