Amount of alcohol breast cancer

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Links between alcohol consumption and breast cancer: a look at the evidence

Leadership alcohol problems estrogen bowlers in the international. Subtly, better understanding of how much information increases quarterly cancer treatment is crucial for medical massage cancer prevention strategies. Ones rests, although observational — outlet they were on antics from handbags - have not found an increased exposure of breast cancer associated with deep dark.

Cell culture, animal, and human studies reveal multiple plausible pathways by which alcohol may play a role in breast cancer pathogenesis [ 53 ]. The most commonly explored pathways stem from both the carcinogenic role of ethanol metabolites as well as the role of alcohol in altering estrogen levels [ 1 - 4 ]. Acetaldehyde AA is the primary ethanol metabolite suggested to have a possible role in breast cancer pathogenesis. Moreover, by decreasing the availability of methyl donors, it can indirectly modify epigenetic histones and DNA methylation creating genomic instability [ 2315 ]. Higher intake of alcohol has also been shown to increase circulating estrogen levels reviewed in [ 142 ].

Estrogen is thought to induce hormone-receptor mediated cell proliferation and cause genetic alterations including aneuploidy [ 24 ]. Importantly, as alcohol has been associated with breast cancer risk in both case-control and cohort studies reviewed in [ 31 ]it is less likely that selection bias or information bias are plausible explanations for this association as these two biases operate differently in these study designs. Mammary adenocarcinomas were induced in rats continuously exposed to supraphysiological doses of estrogens, while fibroadenomas were found in rats dosed with low estrogen levels over long periods of time [ 8384 ].

In premenopausal adult women, alcohol intake has been associated with higher circulating levels of estradiol and estrone [ 90 — 92 ]. The alcohol-related increase in plasma estradiol was restricted to women using oral contraceptives in another controlled diet study [ 94 ]. In addition, a shorter menstrual cycle was reported by premenopausal women with moderate alcohol consumption as compared with nondrinkers, suggesting an increased exposure to endogenous estrogens [ 95 ].

For adolescent girls, the impact brreast alcohol consumption on sex hormone levels remains unclear. In contrast, Block et al. A recent meta-analysis of eight prospective studies among postmenopausal women showed that alcohol intake is positively associated with all the sex hormones, with the strongest association for dehydroepiandrosterone sulfate DHEASbut inversely associated with sex hormone-binding globulin [ 98 ]. DHEAS is an androgen and can be metabolized to estrogen in the breast by aromatase. There is an even more pronounced Amoint of moderate alcohol intake on blood estradiol levels in post-menopausal women who were taking HT.

Compared alcobol nondrinkers using estrogen, cancfr women who consumed Alcohol may increase circulating allcohol hormone levels or an increase in the hepatic Aomunt state and inhibition of a,cohol activity of sulfotransferase and 2-hydroxylase, resulting in a decrease in steroid degradation [ 94]. Another explanation is the akcohol aromatase activity following chronic alcohol consumption, which leads to an enhanced conversion of testosterone to estrogens []. The elevated levels of intracellular estrogens resulting from alcohol intake may act through the ER to promote breast tumor growth.

Several epidemiologic studies have shown that alcohol was more strongly associated with hormone-receptor-positive breast tumors than with other types of breast cancer [ 10 ], consistent with an underlying hormonal basis for the association between alcohol intake and breast cancer. Together, these results support the hypothesis that alcohol may enhance breast tissue's sensitivity to estrogens and predominantly increase the risk of breast cancer expressing the hormone receptors. Alcohol metabolism The ethanol-induced increase in sex hormones is thought to promote proliferation of already initiated mammary epithelial cells but not cause neoplastic transformation of normal epithelial cells [ ].

Another possibility is related to carcinogenic products of alcohol metabolism. In the human body, alcohol is converted to acetaldehyde primarily by alcohol dehydrogenase and further to acetate by acetaldehyde dehydrogenase and xanthine oxidoreductase [ 5]. In addition, acetaldehyde inhibits the repair of oxidative DNA damages induced by alkylating agents [ ]. Although liver is a primary site where acetalde-hyde and free radicals are produced in the process of alcohol metabolism, normal human breast tissue has the capacity to metabolize ethanol at low concentrations and alcohol dehydrogenase is expressed in the human breast epithelial cells [ 9].

In rats, acetalde-hyde accumulates in mammary tissue for prolonged periods of time after a single oral dose of ethanol and finally reaches a level considerably higher than in blood []. This is primarily due to increasing production of acetaldehyde in mammary tissue, the limited ability to detoxify acetaldehyde in mammary tissue and acetaldehyde produced elsewhere and delivered to mammary tissue via blood [ ]. In addition to acetaldehyde, reactive oxygen species ROS are derived from alcohol metabolism and have been implicated in alcohol-associated breast carcinogenesis.

ROS are involved in both the initiation and progression of cancer [ ]. Xanthine oxidoreductase and aldehyde oxidase, two enzymes involved in acetaldehyde metabolism, can generate ROS and are also present in mammary tissue [ ]. Thus, exposure to alcohol may increase oxidative DNA damage in breast tissue. This hypothesis is supported by a recent in vitro study in which alcohol-derived salsolinol significantly enhanced 8-oxo-dG formation, an indicator of oxidative damage, in normal mammary epithelial cells [ ]. Elevated levels of 8-oxo-dG adducts in DNA play a fundamental role in breast cancer [ ].

Other mechanisms The EMT is essential for the normal development and also emerging as an important mechanism for cancer progression [ ]. During the EMT, epithelial cells lose their polarity and tight cell—cell adhesion, and gain migratory and invasive properties to become mesenchymal cells.

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The ethanol concentrations used in this study were equivalent to those that could be generated by moderate alcohol intake in humans. Carcinogenic effects of ethanol may not only target breast epithelial cells. Ethanol may also affect stromal cells and interfere with the tumor—stroma interaction. MMPs enhance tumor invasion and metastasis by degrading the extracellular matrix and promoting cell migration [ ]. High levels of MMP-2 and MMP-9 expression in tumor tissue have been correlated with enhanced metastasis and poor prognosis in breast cancer patients [ — ].

In most cases, these two MMPs are not produced by malignant epithelial cells, but by surrounding tumor stroma, particularly stromal fibroblasts [].

Alcohol breast of cancer Amount

Ethanol activates MMP-2 production by fibroblasts in a dose-dependent manner and culture medium collected from ethanol-exposed fibroblasts significantly alters the invasive behavior of breast cancer cells and mammary epithelial cells [ ]. In addition, a recent in vitro study showed that ethanol promotes the adhesion of breast cancer cells to fibronectin, an important component of the extracellular matrix through suppression of the Nm23 meta-static suppressor gene and subsequent enhancement of fibronectin receptor ITGA5 expression [ ]. Ethanol stimulates migration and invasion of breast cancer cells [ ], particularly those overexpressing HER2 [ ].

Emerging evidence suggests the impact of alcohol on epigenetic regulation of gene expression [ ]. Epigenetic dysregulation is a key mechanism for tumor initiation and progression. Abnormal DNA methylation is the best understood epigenetic cause of disease. Global hypomethylation can result in chromosome instability, and region-specific hypermethylation has been linked with the silencing of tumor suppressor genes. Chronic alcohol intake has been Amount of alcohol breast cancer to lower leukocyte DNA global methylation in humans [ ].

In a study of the methylation profiles of breast tumors, Christensen et al. There were no individual CpG loci showing statistically significant alcohol-related changes in methylation in that study. A drink is defined as 12 ounces of beer, 5 ounces of wine or 1. If you choose to drink, exceeding the recommended limit of one alcoholic drink a day increases your breast cancer risk. These studies, although observational — meaning they draw on inferences from researchers - have consistently found an increased risk of breast cancer associated with alcohol intake. How does alcohol affect breast cancer risk? When we do this, we don't see a strong pattern one way or the other. That is, some studies show alcohol slightly increases risk of breast cancer recurrence, while others show it decreases risk.

This suggests that if there is an effect of alcohol, it is probably very small, regardless of whether it is protective or harmful. And if alcohol does turn out to increase risk of recurrence after breast cancer, the studies suggest the effect is likely to be strongest for overweight and obese women. If you have a history of breast cancer, are at high risk of developing breast cancer due to genetic or other factors, or you are significantly overweight, you might consider saving alcohol for special occasions, or enjoying it once per week with a nice dinner. If completely avoiding alcohol is not difficult for you, you may decide it's easiest to simply avoid it.

Alcohol also may increase breast cancer risk by damaging DNA in cells. Teen and tween girls aged 9 to 15 who drink three to five drinks a week have three times the risk of developing benign breast lumps. Certain categories of non-cancerous breast lumps are associated with a higher risk of breast cancer later in life. All types of alcohol count. One drink equals 12 ounces of beer, 5 ounces of wine, or 1.

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