Medical hypothesis: bifunctional genetic-hormonal pathways to breast cancer

Environmental Health Perspectives
D L DavisH L Bradlow

Abstract

As inherited germ line mutations, such as loss of BRCA1 or AT, account for less than 5% of all breast cancer, most cases involve acquired somatic perturbations. Cumulative lifetime exposure to bioavailable estradiol links most known risk factors (except radiation) for breast cancer. Based on a series of recent experimental and epidemiologic findings, we hypothesize that the multistep process of breast carcinogenesis results from exposure to endogenous or exogenous hormones, including phytoestrogens that directly or indirectly alter estrogen metabolism. Xenohormones are defined as xenobiotic materials that modify hormonal production; they can work bifunctionally, through genetic or hormonal paths, depending on the periods and extent of exposure. As for genetic paths, xenohormones can modify DNA structure or function. As for hormonal paths, two distinct mechanisms can influence the potential for aberrant cell growth: compounds can directly bind with endogenous hormone or growth factor receptors affecting cell proliferation or compounds can modify breast cell proliferation altering the formation of hormone metabolites that influence epithelial-stromal interaction and growth regulation. Beneficial xenohormones, such as indole-3-car...Continue Reading

References

Jan 1, 1992·Acta Oncologica·H AdlercreutzK Höckerstedt
Jul 30, 1992·The New England Journal of Medicine·J R HarrisW Willett
Jan 1, 1990·Annals of the New York Academy of Sciences·L KohlmeierH Hoffmeister
Nov 1, 1990·Endocrine Reviews·J J Li, S A Li
Sep 1, 1988·The American Journal of Clinical Nutrition·B R Goldin, S L Gorbach
Nov 1, 1988·Proceedings of the National Academy of Sciences of the United States of America·G E Swaneck, J Fishman
May 1, 1982·European Journal of Cancer & Clinical Oncology·B S ThomasR R Millis
Oct 1, 1981·The Journal of Clinical Endocrinology and Metabolism·J H MacIndoe, L A Etre
Sep 26, 1995·Proceedings of the National Academy of Sciences of the United States of America·J G LiehrB T Zhu
Feb 1, 1995·Journal of the National Cancer Institute·P G TonioloB S Pasternack
Apr 25, 1995·Proceedings of the National Academy of Sciences of the United States of America·S NandiJ Yang
Jun 6, 1995·Proceedings of the National Academy of Sciences of the United States of America·B N AmesW C Willett
Oct 1, 1993·Environmental Health Perspectives·D L DavisH Anton-Culver
Jan 19, 1994·Journal of the National Cancer Institute·R K TiwariM P Osborne
Sep 30, 1995·Annals of the New York Academy of Sciences·J FishmanN T Telang
Apr 16, 1996·Proceedings of the National Academy of Sciences of the United States of America·J G Liehr, M J Ricci
Apr 30, 1996·Annals of the New York Academy of Sciences·N T Telang
Apr 1, 1997·Environmental Health Perspectives·C DeesC M Ardies
Dec 1, 1948·The British Journal of Radiology·J CLEMMESEN

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Citations

Aug 29, 1998·Environmental Health Perspectives·D L DavisA J Sasco
Aug 2, 2001·APMIS : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica·J L SpearowM Barkley
Feb 13, 2001·The Journal of Steroid Biochemistry and Molecular Biology·L H KullerE N Meilahn
Oct 18, 2002·International Journal of Cancer. Journal International Du Cancer·Montserrat García-ClosasJoanne F Dorgan
Nov 4, 2008·Mutation Research·Salvador MenaJosé M Estrela
Sep 25, 2008·International Journal of Cancer. Journal International Du Cancer·Barbara NemesureUNKNOWN Barbados National Cancer Study Group
Jul 6, 2005·Mutation Research·Marta CasellaSilvia Maffei
Apr 13, 2000·Journal of Clinical Epidemiology·A P HøyerP Grandjean
May 21, 2013·Chemical Research in Toxicology·Daniel M RotroffRichard S Judson
Feb 24, 1998·Annals of the New York Academy of Sciences·D L DavisM Wolff
Feb 18, 2017·International Journal of Molecular Sciences·Farrukh AqilRamesh C Gupta
Nov 7, 2019·Journal of Cellular Biochemistry·Wen-Jing LiuSheng-Xiang Lin
May 11, 2002·The Proceedings of the Nutrition Society·Miriam N Jacobs, David F V Lewis
Nov 27, 2002·The American Journal of Clinical Nutrition·Sidika E Kasim-KarakasBill L Lasley
Nov 25, 2003·The Journal of Steroid Biochemistry and Molecular Biology·Jose RussoIrma H Russo

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