Inflammation, atrophy, and prostate carcinogenesis

Urol Oncol. 2007 Sep-Oct;25(5):398-400. doi: 10.1016/j.urolonc.2007.05.007.

Abstract

The etiological agents that cause prostate cancer remain unknown. There is emerging evidence that "risk factor" lesions that are proposed to represent regenerative epithelium in response to environmental insults may precede the development of prostatic intraepithelial neoplasia and early carcinoma. Recent evidence suggests that these lesions, referred to collectively as proliferative inflammatory atrophy, may arise in the setting of inflammation and dietary toxins, such as "charred meat" carcinogens. Additional epidemiological, molecular pathological, and animal model work needs to be done to determine whether inflammation and atrophy are "driving" prostate carcinogenesis.

Publication types

  • Review

MeSH terms

  • Animals
  • Atrophy / chemically induced*
  • Carcinogens, Environmental / chemistry
  • Carcinogens, Environmental / toxicity*
  • Cattle
  • Cell Transformation, Neoplastic / chemically induced*
  • Cell Transformation, Neoplastic / pathology
  • Chronic Disease
  • Food Handling
  • Heterocyclic Compounds / chemistry
  • Heterocyclic Compounds / toxicity
  • Humans
  • Imidazoles / chemistry
  • Imidazoles / toxicity
  • Male
  • Meat / poisoning
  • Models, Biological
  • Prostatic Neoplasms / etiology*
  • Prostatic Neoplasms / pathology*
  • Prostatitis / chemically induced*
  • Rats
  • Risk Factors
  • Temperature

Substances

  • Carcinogens, Environmental
  • Heterocyclic Compounds
  • Imidazoles
  • 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine