Accession Number:

ADB261109

Title:

Estrogen Metabolism and Prostate Cancer Risk

Descriptive Note:

Annual rept.1 Oct 1998-30 Sep 1999

Corporate Author:

STATE UNIV OF NEW YORK AT BUFFALO AMHERST

Personal Author(s):

Report Date:

1999-10-01

Pagination or Media Count:

46.0

Abstract:

Environmental factors such as sedentary life-style and high fat diet have been associated with an increase in prostate cancer risk . An explanation of the linkage between the environmental factors and prostate cancer risk might be the of these factors on hormone metabolism, in particular estrogen metabolism. For instance, there is experimental evidence showing that a sedentary life-style and high fat diet induce estrogen metabolism toward l6alpha hydroxylation leading to biologically potent metabolites estriol and 16alpha hydroxyestrone. An active life-style and a low fat diet induce the alternative 2-hydroxylation with production of weak estrogen metabolites 2-hydroxyestrone. Potent estrogens may increase prostate cell division and increase prostate cancer risk. The research hypothesis is that the preferential induction of the l6alpha hydroxylation pathway in respect to the 2- hydroxylation, is associated with an increase risk of prostate cancer. To test this hypothesis a population based case control study is conducted. Men age 50-79, African American and white, residents Erie and Niagara Counties in Western New York, with incident, pathologically confirmed prostate cancer are interviewed. Controls are interviewed as part of other funded on-going case-control studies and randomly selected from the general population. Urine is used for the determinations of the l6alpha and 2- hydroxyestrone. Diet, physical activity, and possible confounders are also evaluated in relation to the estrogen pathways and include in the final evaluation of the association between estrogen metabolism and prostate cancer risk.

Subject Categories:

  • Anatomy and Physiology
  • Medicine and Medical Research
  • Food, Food Service and Nutrition

Distribution Statement:

APPROVED FOR PUBLIC RELEASE