16 alpha-hydroxylation of estradiol: a possible risk marker for breast cancer

Ann N Y Acad Sci. 1986;464:138-51. doi: 10.1111/j.1749-6632.1986.tb16001.x.

Abstract

From these results we may conclude that estradiol 16 alpha-hydroxylation is highly correlated with tumor incidence, and that the reaction is partly regulated by MMTV and the rest by genetic influences. Elevated hydroxylation appears to be an autosomal dominant trait that is highly specific for estradiol. It is also pertinent that the product of the 16 alpha-hydroxyestrone reaction is a potent estrogen that is capable of binding covalently to amino acids and nucleotides, including the estrogen receptor molecule. The results obtained in these studies establish the usefulness of the mouse model for studying the interrelationship between enhanced 16-hydroxylation of estradiol and the incidence of mammary tumors.

Publication types

  • Comparative Study
  • Review

MeSH terms

  • Age Factors
  • Animals
  • Breast / analysis
  • Breast Neoplasms / analysis*
  • Dihydrotestosterone / metabolism
  • Estradiol / analogs & derivatives
  • Estradiol / analysis
  • Estradiol / metabolism*
  • Estriol / analysis*
  • Female
  • Haplorhini
  • Humans
  • Hydroxylation
  • Male
  • Mammary Glands, Animal / analysis
  • Mammary Neoplasms, Experimental / analysis
  • Mammary Tumor Virus, Mouse / analysis
  • Mice
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Pan troglodytes
  • Pregnenolone / metabolism
  • Progesterone / metabolism
  • Rats
  • Risk
  • Species Specificity
  • Steroid 16-alpha-Hydroxylase
  • Testosterone / metabolism

Substances

  • Dihydrotestosterone
  • Testosterone
  • Progesterone
  • Estradiol
  • Pregnenolone
  • 2-hydroxyestradiol
  • Steroid 16-alpha-Hydroxylase
  • Estriol