Cancer and Metastasis Reviews

, Volume 21, Issue 1, pp 3–16

The Diet, Prostate Inflammation, and the Development of Prostate Cancer


  • William G. Nelson
    • The Sidney Kimmel Cancer Center at Johns Hopkins
  • Theodore L. DeWeese
    • The Sidney Kimmel Cancer Center at Johns Hopkins
  • Angelo M. DeMarzo
    • The Sidney Kimmel Cancer Center at Johns Hopkins

DOI: 10.1023/A:1020110718701

Cite this article as:
Nelson, W.G., DeWeese, T.L. & DeMarzo, A.M. Cancer Metastasis Rev (2002) 21: 3. doi:10.1023/A:1020110718701


Evidence that somatic inactivation of GSTP1, encoding the human π-class glutathione S-transferase, may initiate prostatic carcinogenesis is reviewed along with epidemiological evidence implicating several environment and lifestyle factors, including the diet and sexually transmitted diseases, as prostate cancer risk factors. An integrated model is presented featuring GSTP1 function as a 'caretaker' gene during the pathogenesis of prostate cancer, in which the early loss of GSTP1 activity renders prostate cells vulnerable to genome damage associated with chronic prostatic inflammation and repeated exposure to carcinogens. The model predicts that the critical prostate carcinogens will be those that are substrates for GSTP1 detoxification and are associated with high prostate cancer risk diet and lifestyle habits.

prostate cancerglutathione S-transferasesproliferative inflammatory atrophyoxidative stress

Copyright information

© Kluwer Academic Publishers 2002