The diet, prostate inflammation, and the development of prostate cancer

Cancer Metastasis Rev. 2002;21(1):3-16. doi: 10.1023/a:1020110718701.

Abstract

Evidence that somatic inactivation of GSTP1, encoding the human pi-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 GSTPI function as a 'caretaker' gene during the pathogenesis of prostate cancer, in which the early loss of GSTPI 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.

Publication types

  • Review

MeSH terms

  • Cell Transformation, Neoplastic
  • Chromosome Aberrations
  • Diet*
  • Disease Progression
  • Glutathione S-Transferase pi
  • Glutathione Transferase / physiology
  • Humans
  • Isoenzymes / physiology
  • Male
  • Oxidative Stress
  • Prostatic Neoplasms / enzymology
  • Prostatic Neoplasms / etiology*
  • Prostatic Neoplasms / prevention & control
  • Prostatitis / enzymology
  • Prostatitis / etiology*
  • Risk Factors

Substances

  • Isoenzymes
  • GSTP1 protein, human
  • Glutathione S-Transferase pi
  • Glutathione Transferase