Role of Estrogen in Alcohol Promotion of Breast Cancer and Prolactinomas

Sarkar, Dipak K.; Liehr, Joachim G.; Singletary, Keith W.

doi:10.1097/00000374-200105051-00037

Cited by 8 publications

(6 citation statements)

References 79 publications

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“…The interaction of chronic alcohol intake with estrogen has been recognized in prolactinomas; however, the potential mechanism has not been clearly defined (Sarkar et al 2001). The present results demonstrated that a very low concentration of ethanol (0.01%) stimulated ERα signaling but suppressed the actions of 17β-estradiol (E2) in the rat pituitary somatolactotrope GH4C1 (GH4) cell line.…”

Section: Discussionmentioning

confidence: 55%

“…Conversely, alcohol is also positively associated with the occurrence of cancers of various organs, particularly in postmenopausal women (Lieber et al 1979;Blot 1992;Singletary and Gapstur 2001;Pöschl and Seitz 2004;Boffetta and Hashibe 2006;Seitz and Stickel 2007). Alcoholic men frequently exhibit evidence of feminization, as manifested in gynecomastia, spider angiomata, palmar erythema, and changes in body hair pattern (Sarkar et al 2001). The mechanisms underlying these diverse effects are thought to be mediated by estrogen, since alcohol has been found, although not invariably, to elevate plasma estrogen levels (Ginsburg 1999;Purohit 2000;Singletary and Gapstur 2001).…”

mentioning

confidence: 99%

“…Alcohol consumption is strongly associated with prolactin-secreting adenomas (prolactinomas) and hyperprolactinemia (Sarkar et al 2001). However, the mechanisms of alcohol-induced carcinogenesis are still elusive.…”

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confidence: 99%

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Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

et al. 2009

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The interaction of chronic alcohol consumption with estrogen has been recognized in various tissues; however, the potential mechanism has not been clearly defined. In this study, we made the following observations: (a) 0.01% (v/v) ethanol (corresponding to 1.7 mM) significantly elevated estrogen receptor alpha (ERalpha) protein content, stimulated activator protein-1 (AP-1)-dependent ERalpha transcriptional activities, and ultimately enhanced GH4C1 cells growth in vitro and (b) the same concentration of ethanol suppressed the stimulatory effects of 17beta-estradiol (E2; 10 nM) on both cell growth and cellular PRL accumulate through attenuation of ERalpha actions at both the estrogen response element and the AP-1 site. These observations raise the question as to what extent ethanol influences signal transduction pathways controlled by E2 in experimental medicine and biology.

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Section: Discussionmentioning

confidence: 55%

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confidence: 99%

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Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

et al. 2009

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“…Like estradiol, ethanol reduces the activity of the growth-inhibitory TGF-␤1 and stimulates the activity of TGF-␤3 in the pituitary gland. Hence, it is hypothesized that ethanol may promote prolactinomas by controlling the cell-regulatory processes in the lactotropes and/or by enhancing the action of estrogen on the lactotropes [125].…”

Section: Alcohol and Estrogen Statusmentioning

confidence: 99%

Alcohol drinking and breast cancer

Barber

Shields

2006

Breast Cancer Online

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Breast cancer is a multifactorial disease that is triggered by gene-environment interactions. Epidemiological research has identified alcohol consumption as a significant non-hormonal-related and consistent risk factor, and is thus a preventable cause of breast cancer. The reasons why alcohol drinking increase breast cancer risk are unclear, and several hypotheses exist. The perturbation of estrogen metabolism and response appears to one mechanism underlying the association. Alcohol consumption also increases breast density in postmenopausal women and affects sex steroid levels. Other plausible mechanisms include: (1) mutagenesis by acetaldehyde, which is a metabolite of ethanol; (2) by enhancing the susceptibility of the mammary gland to carcinogenesis by affecting DNA repair, stimulating cell proliferation or altering mammary gland structural development; (3) influencing the disposition and function of essential nutrients or dietary factors considered cancer protective (e.g. affecting folate and one-carbon metabolism pathways); (4) inducing genome instability and DNA damage; and (5) inducing oxidative damage via ethanol or estrogen metabolism. To better understand the etiological nature of the effect of alcohol on breast carcinogenesis, further studies at the cellular and molecular levels on the interaction between ethanol and other risk factors, estrogen, carcinogens are needed.

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“…As little as 5-6 g of daily alcohol intake has been found to significantly increase the risk of developing breast cancer [5] and breast cancer recurrence [3,6]. Mechanisms responsible for the increased risk may be due to increased estrogen and androgen levels [7,8] or increased levels of plasma insulin-like growth factors produced by the liver following alcohol consumption [9]. In addition, alcohol-related breast cancer risk may be compounded for individuals who have other lifestyle risk factors, such as obesity [6].…”

Section: Introductionmentioning

confidence: 99%

Alcohol Intake Among Breast Cancer Survivors: Change in Alcohol Use During a Weight Management Intervention

2016

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BackgroundDaily alcohol intake in quantities as small as half a drink/day significantly increases the risk of breast cancer recurrence for postmenopausal survivors. Interventions designed to modify alcohol use among survivors have not been studied; however, lifestyle interventions that target change in dietary intake may affect alcohol intake.ObjectiveTo evaluate change in alcohol use during a weight loss intervention for obese, rural-dwelling breast cancer survivors.MethodsData were derived from an 18-month trial that included a 6-month weight loss intervention delivered via group conference calls, followed by a 12-month randomized weight loss maintenance phase in which participants received continued group calls or mailed newsletters. Participants who reported regular alcohol use at baseline (N=37) were included in this study.ResultsMean daily alcohol intake significantly decreased from baseline to 6 months during the weight loss intervention (19.6-2.3 g; P=.001). Mean alcohol intake did not significantly increase (b=0.99, P=.12) during the weight loss maintenance phase (months 6-18) and did not depend on randomization group (b=0.32, P=.799).ConclusionsFindings provide preliminary evidence that a weight loss intervention may address obesity and alcohol use risk factors for cancer recurrence. Minimal mail-based contact post weight loss can maintain alcohol use reductions through 18 months, suggesting durability in these effects. These results highlight a possibility that lifestyle interventions for survivors may modify health behaviors that are not the main foci of an intervention but that coincide with intervention goals.Trial RegistrationClinicaltrials.gov NCT01441011; https://clinicaltrials.gov/ct2/show/NCT01441011 (Archived by WebCite at http://www.webcitation.org/6lsJ9dMa9)

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Role of Estrogen in Alcohol Promotion of Breast Cancer and Prolactinomas

Cited by 8 publications

References 79 publications

Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

Alcohol drinking and breast cancer

Alcohol Intake Among Breast Cancer Survivors: Change in Alcohol Use During a Weight Management Intervention

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