The interaction between HPV infection and estrogen metabolism in cervical carcinogenesis

Int J Cancer. 1991 Dec 2;49(6):867-9. doi: 10.1002/ijc.2910490611.


Cancer of the genital tract is the final outcome of some infections with human papillomavirus (HPVs), and the most estrogen-sensitive cells are at greatest risk for the HPV-related cancers. Therefore we investigated relationships between HPVs and estrogen metabolism in cells of the genital tract. Increased conversion of estradiol to 16 alpha-hydroxyestrone, known to be a risk factor for cancer in some other estrogen-sensitive cells, was investigated in keratinocytes from the genital tract. Primary cells, particularly those explants from the transformation zone of the cervix, are able to 16 alpha-hydroxylate estradiol. Both cervical and foreskin cells immortalized with HPV-16 are greatly enhanced in the 16 alpha-hydroxylation of estradiol as compared with normal cells. We suggest a model whereby the combined action of 16 alpha-hydroxylation of estrogen and HPV work together to promote cell proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aryl Hydrocarbon Hydroxylases*
  • Biotransformation
  • Cell Line, Transformed
  • Cells, Cultured
  • Cervix Uteri / metabolism
  • Cytochrome P-450 CYP2C8
  • Cytochrome P-450 CYP2C9
  • Estrogens / metabolism*
  • Female
  • Humans
  • Keratinocytes / metabolism*
  • Male
  • Papillomaviridae* / genetics
  • Steroid 16-alpha-Hydroxylase
  • Tumor Virus Infections / complications*
  • Uterine Cervical Neoplasms / etiology*


  • Estrogens
  • CYP2C9 protein, human
  • Cytochrome P-450 CYP2C9
  • Aryl Hydrocarbon Hydroxylases
  • CYP2C8 protein, human
  • Cytochrome P-450 CYP2C8
  • Steroid 16-alpha-Hydroxylase