Estrogen metabolism and breast cancer

Abstract

There is currently accumulating evidence that endogenous estrogens play a critical role in the development of breast cancer. Estrogens and their metabolites have been studied in both pre- and postmenopausal women with more consistent results shown in the latter population, in part because of large hormonal variations during the menstrual cycle and far fewer studies having been performed in premenopausal women. In this review we describe in detail estrogen metabolism and associated genetic variations, and provide a critical review of the current literature regarding the role of estrogens and their metabolites in breast cancer risk.

Night shift work and other determinants of estradiol, testosterone, and dehydroepiandrosterone sulfate among middle-aged nurses and midwives

“…Both experimental and observational studies confirmed the role of estrogens in the etiology of breast cancer (4). Strong epidemiological evidence for the association between circulating estrogens and breast cancer was established among postmenopausal women, although this relationship was less convincing among premenopausal women (5,6). Also, increased circulating concentrations of dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS) and testosterone were associated with breast cancer risk among women (5,7).…”

Apoptotic Bax Gene Expression in Glioblastoma Cells Exposed to Estradiol valerate

“…It has been shown that estrogen has critical role in development of breast cancer [12]. Greater exposure to estrogens may be a risk factor for thyroid cancer [13].…”

Acetylation targets HSD17B4 for degradation via the CMA pathway in response to estrone

“…E2 is the most potent and active form of estrogen, whereas E1 is the less active form of estrogen. HSD17B1 (17b-hydroxysteroid dehydrogenase1) is the most active enzyme to produce E2 [7][8][9][10] and significantly overexpressed in breast cancer, which contributes to the stimulation and development of breast cancer., 11,12 HSD17B2, which converts E2 to E1, is dominant in normal breast. 13 Studies have shown that increased HSD17B1 expression or ratio of HSD17B1 and HSD17B2 expression is associated with poor clinical outcome of estrogen-dependent breast cancer patients.…”