The diet, prostate inflammation, and the development of prostate cancer.
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.
Nelson
William G
WG
The Sidney Kimmel Cancer Center at Johns Hopkins, Baltimore, MD, USA.
DeWeese
Theodore L
TL
DeMarzo
Angelo M
AM
D002471:Cell Transformation, Neoplastic; D002869:Chromosome Aberrations; D004032:Diet; D018450:Disease Progression; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase / Q000502:physiology; D006801:Humans; D007527:Isoenzymes / Q000502:physiology; D008297:Male; D018384:Oxidative Stress; D011471:Prostatic Neoplasms / Q000201:enzymology / Q000209:etiology* / Q000517:prevention & control; D011472:Prostatitis / Q000201:enzymology / Q000209:etiology*; D012307:Risk Factors
D007527:Isoenzymes; C496556:GSTP1 protein, human; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase