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Genetic susceptibility and environmental estrogen-like compounds
V N Kristensen1, E H Kure, B Erikstein
1Department of Genetics, Institute of Cancer Research, The Norwegian Radium Hospital, Montebello 0310, Oslo, Norway. nedelcheva.vessela@dnr.uio.no
Mutation Research
|September 6, 2001
Summary
Environmental estrogens may impact the endocrine system. Genetic variations in key estrogen-synthesizing enzymes could influence breast cancer risk, affecting how individuals respond to these hormone-like substances.
Area of Science:
- Endocrinology
- Environmental Health
- Oncology
Background:
- Environmental chemicals can possess estrogenic activity, potentially disrupting the endocrine system.
- Estrogen synthesis occurs in specific cells (ovarian theca, breast adipose) and tissues, utilizing a range of enzymes.
- Breast tissue expresses enzymes crucial for both estrogen synthesis and metabolism.
Purpose of the Study:
- To explore the potential role of genetic polymorphisms in estrogen-metabolizing enzymes.
- To investigate the link between environmental estrogens and breast cancer risk.
- To understand interindividual variations in susceptibility to hormone-like substances.
Main Methods:
- Analysis of enzyme expression in relevant human tissues.
- Review of literature on environmental estrogens and endocrine disruption.
- Examination of genetic polymorphisms in key steroidogenic enzymes (e.g., CYP17, CYP19, COMT).
Main Results:
- Identified key enzymes (CYP17, CYP11a, CYP19, 17-beta-hydroxysteroid dehydrogenase, steroid sulfatase, CYP1A1, CYP3A4, CYP1B1, COMT) involved in estrogen synthesis and metabolism.
- Highlighted the presence of these enzymes in ovarian theca cells, breast adipose stromal cells, and breast tissue.
- Suggested that polymorphisms in these enzymes may modify breast cancer risk.
Conclusions:
- Genetic variations in enzymes regulating estrogen pathways may influence breast cancer risk.
- Interactions between environmental estrogens and individual genetic makeup are critical.
- Further research is warranted to elucidate the precise mechanisms linking genetic polymorphisms, environmental exposures, and cancer development.