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

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)3-16
Number of pages14
JournalCancer and Metastasis Reviews
Volume21
Issue number1
DOIs
StatePublished - 2002

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Prostate
Prostatic Neoplasms
Diet
Inflammation
Carcinogens
Life Style
Feeding Behavior
Sexually Transmitted Diseases
Glutathione Transferase
Carcinogenesis
Genome
Genes

Keywords

  • Glutathione S-transferases
  • Oxidative stress
  • Proliferative inflammatory atrophy
  • Prostate cancer

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

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abstract = "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.",
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AB - 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.

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