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Dhea and breast cancer

Dhea and breast cancer

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In conclusion In vitro and in vivo studies have shown that dehydroepiandrosterone (DHEA) inhibits the development of mammary carcinomas. Very high levels of DHEA and/or dehydroepiandrosterone sulfate (DHEAS) have been identified in breast tissues and secretions in humans, and epidemiological studies indicate that these steroids may play a role in breast cancer growth modulation. While both an absorption from plasma and a transformation from precursors have been proposed, the primary source of the adrenal C19 steroids present in the breast is still unknown. In an attempt to explain this point, we looked at: a) DHEAS and DHEA concentrations in tumor tissue; b) differences in DHEAS (or DHEA) concentration in peripheral venous plasma and that draining the affected breast, which we think represent the arteriovenous gradient of these steroids; and c) DHEA sulfatase production in tumor tissue in ten patients who had breast cancer surgery. DHEA sulfatase activity is unrelated to DHEAS or DHEA concentrations in breast cancer tissue, according to the findings. DHEA levels of blood supplying and draining the breast with cancer are not different, revealing a negative DHEA plasma gradient around the breast. The concentration of DHEA in tumor tissue is positively linked to the DHEA plasma gradient across the breast. The data support the hypothesis that plasma contributes a significant amount of DHEA to DHEA present in breast cancer tissue.

#42–avrum bluming, m.d. and carol tavris, ph.d.: a

Biomarker analysis (androgen receptor, estrogen receptor, progesterone receptor, HER2/neu, Ki-67, and p53) is performed on tissue samples taken at baseline and during surgery. Serum hormone (e.g., estrone, estradiol, testosterone, dihydrotestosterone, DHEA, and DHEA-sulfate) and cytokine levels are measured in blood samples taken at baseline and after DHEA treatment is completed.
Day 14 (approximately 2 weeks prior to surgery): start a 2-week course of DHEA; Day 7 (approximately 1 week after starting treatment): answer question about pill diary; Day 0 (approximately 2 weeks after starting treatment, within 48 hours prior to surgery): start a 2-week course of DHEA; Day 0 (approximately 2 weeks after starting treatment, within 48 hours prior to surgery): start a 2-week course of DHE
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Ignacio Chávez, México YASMN NANSI ORTEGA-CALDERN Laboratory of Cell Biology, Department of Physiology, National Institute of Cardiology

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REBECA LPEZ-MARURE Department of Physiology, National Institute of Cardiology, Ignacio Chávez, México REBECA LPEZ-MARURE Laboratory of Cell Biology, Department of Physiology, National Institute of Cardiology, Ignacio Chávez, México
Dehydroepiandrosterone (DHEA), an adrenal steroid present at the highest concentration in human plasma, has been shown to protect against a number of cancers, but its mechanisms of action are unclear. We looked at how DHEA affected the proliferation and migration of three cervical cancer cell lines. Crystal violet staining was used to assess cell proliferation, and attachment, transwell, and wound assays were used to assess cell migration. With a half-maximal inhibitory concentration (IC50) of 30 M, DHEA inhibited the proliferation of InBl and SiHa cells, while an IC50 of 70 M inhibited the proliferation of HeLa cells. DHEA inhibited cell attachment to the plastic surface of the culture wells at these IC50s, and migration was measured using transwells after 24 hours of exposure. DHEA also inhibited the three cell lines from migrating into the wound. These findings point to the inhibition of tumor cell proliferation and migration as a potential mechanism for DHEA’s defense against cervical cancer. Cervical cancer can benefit from DHEA treatment or prevention.

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Androgens have significant physiological effects in women while also being suspected of being involved in breast cancer pathologies. However, there is some disagreement about the impact of androgens on mammary epithelial proliferation and/or breast cancer incidence. We conducted a review of the literature to assess existing clinical, genetic, and epidemiological evidence on androgens’ function in mammary growth and neoplasia. Epidemiological trials tend to have major methodological defects, resulting in contradictory findings. The research into androgenic pathway-related molecular defects in breast cancer is still in its early stages. Androgens appear to prevent mammary epithelial proliferation and breast development in humans and nonhuman primates, whereas estrogen therapy suppresses endogenous androgens. Androgens are thought to naturally inhibit mammary epithelial proliferation and breast development, according to a large body of clinical evidence. As a result, androgen suppression with traditional estrogen therapy can increase estrogenic breast stimulation and, potentially, breast cancer risk. The addition of testosterone to a standard hormone therapy regimen can reduce the estrogen/progestin-induced increase in breast cancer risk, but the effect of this combination on mammary gland homeostasis remains to be seen.