5-Alpha-reductase inhibition and prostate cancer prevention

Cancer Epidemiol Biomarkers Prev. 1994 Mar;3(2):177-82.

Abstract

Studies of prostate biology support the concept that dihydrotestosterone is the principal androgen responsible for normal and hyperplastic growth of the prostate gland. Cancer is a process of malignant transformation evolving over time, involving cellular growth and division. Therefore, an altered endocrine state, such as suppression of dihydrotestosterone activity, may have an impact on prostate cells inhibiting carcinogenic transformation. In vitro and in vivo preclinical observations support this hypothesis. A placebo-controlled randomized trial using finasteride, an inhibitor of the enzyme that converts testosterone to dihydrotestosterone, is planned. The endpoint of this trial will be reduction of prostate cancer incidence.

Publication types

  • Review

MeSH terms

  • 3-Oxo-5-alpha-Steroid 4-Dehydrogenase / physiology
  • 5-alpha Reductase Inhibitors*
  • Cell Transformation, Neoplastic / drug effects
  • Cell Transformation, Neoplastic / pathology
  • Dihydrotestosterone / metabolism
  • Humans
  • Male
  • Neoplasms, Hormone-Dependent / mortality
  • Neoplasms, Hormone-Dependent / pathology
  • Neoplasms, Hormone-Dependent / prevention & control*
  • Prostate / pathology
  • Prostatic Neoplasms / mortality
  • Prostatic Neoplasms / pathology
  • Prostatic Neoplasms / prevention & control*
  • Risk Factors
  • Survival Rate

Substances

  • 5-alpha Reductase Inhibitors
  • Dihydrotestosterone
  • 3-Oxo-5-alpha-Steroid 4-Dehydrogenase