Alcohol consumption in relation to aberrant DNA methylation in breast tumors

Tao, Meng Hua; Marian, Cătălin; Shields, Peter G.; Nie, Jing; McCann, Susan E.; Millen, Amy E.; Ambrosone, Christine B.; Hutson, Alan D.; Edge, Stephen B.; Krishnan, Shiva; Xie, Bingteng; Winston, Janet S.; Vito, Dominica; Russell, Marcia; Nochajski, Thomas H.; Trevisan, Maurizio; Freudenheim, Jo L.

doi:10.1016/j.alcohol.2010.11.006

Cited by 29 publications

(23 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The metabolism of alcohol may also result in carcinogenic products and reactive oxygen species (29,30); thus, alcohol may act as a weak carcinogen (7). Recent studies suggest that aberrant DNA methylation patterns (31,32) and interference with epithelium-stroma interactions may also play important roles (33) in alcohol-induced carcinogenesis. The association observed with binge or heavy drinking behaviors also suggests other potential biological mechanisms, including increased inflammation and insulin resistance (9, 10).…”

Section: Discussionmentioning

confidence: 99%

Lifetime Alcohol Intake, Binge Drinking Behaviors, and Breast Cancer Risk

White¹,

DeRoo²,

Weinberg³

et al. 2017

American Journal of Epidemiology

View full text Add to dashboard Cite

The prevalence of binge drinking in the United States is rising. While alcohol is a risk factor for breast cancer, less is known about the impact of episodic heavy drinking. In 2003-2009, women aged 35-74 years who were free of breast cancer were enrolled in the Sister Study (n = 50,884). Residents of the United States or Puerto Rico who had a sister with breast cancer were eligible. Multivariable Cox regression was used to estimate adjusted hazard ratios and 95% confidence intervals for breast cancer. During follow-up (mean = 6.4 years), 1,843 invasive breast cancers were diagnosed. Increased breast cancer risk was observed for higher lifetime alcohol intake (for ≥230 drinks/year vs. <60 drinks/year, hazard ratio (HR) = 1.35, 95% confidence interval (CI): 1.15, 1.58). Relative to lowlevel drinkers (<60 drinks/year), hazard ratios were increased for ever binge drinking (HR = 1.29, 95% CI: 1.15, 1.45) or blacking out (HR = 1.39, 95% CI: 1.17, 1.64). Compared with low-level drinkers who never binged, moderate drinkers (60-229 drinks/year) who binged had a higher risk (HR = 1.25, 95% CI: 1.08, 1.44). There was evidence of effect modification between moderate lifetime drinking and binging (relative excess risk due to interaction = 0.33, 95% CI: 0.10, 0.57). Our findings support the established association between lifetime alcohol intake and breast cancer and provide evidence for an increased risk associated with heavy episodic drinking, especially among moderate lifetime drinkers. alcohol; alcohol drinking; binge drinking; breast cancer Abbreviations: BMI, body mass index; CI, confidence interval; ER, estrogen receptor; HR, hazard ratio; RERI, relative excess risk due to interaction.

show abstract

Section: Discussionmentioning

confidence: 99%

Lifetime Alcohol Intake, Binge Drinking Behaviors, and Breast Cancer Risk

White¹,

DeRoo²,

Weinberg³

et al. 2017

American Journal of Epidemiology

View full text Add to dashboard Cite

show abstract

“…There were no individual CpG loci showing statistically significant alcohol-related changes in methylation in that study. However, other studies reported that alcohol consumption was related to altered methylation patterns for several genes, including hypermethylation of ER-α [139] and tumor suppressor gene E-cadherin and hypomethylation of p16 [140]. …”

Section: Possible Mechanismsmentioning

confidence: 99%

Links between Alcohol Consumption and Breast Cancer: A Look at the Evidence

Liu

Nguyen

Colditz

2015

Womens Health (Lond Engl)

150

112

View full text Add to dashboard Cite

Alcohol consumption by adult women is consistently associated with risk of breast cancer. Several questions regarding alcohol and breast cancer need to be addressed. Menarche to first pregnancy represents a window of time when breast tissue is particularly susceptible to carcinogens. Youth alcohol consumption is common in the USA, largely in the form of binge drinking and heavy drinking. Whether alcohol intake acts early in the process of breast tumorigenesis is unclear. This review aims to focus on the influences of timing and patterns of alcohol consumption and the effect of alcohol on intermediate risk markers. We also review possible mechanisms underlying the alcohol-breast cancer association.

show abstract

“…While methylation levels of some genes in certain tissues may vary with smoking [15], alcohol [15,16], or NSAID [17] use, such exposures did not affect stool levels of the candidate colorectal neoplasia markers studied. These findings suggest that it is not necessary for patients to alter these common lifestyle or medication exposures as preparation for testing by stool DNA assays incorporating these candidate markers.…”

Section: Ndrg4mentioning

confidence: 99%

“…Based on observations across different tissues, rates of aberrant methylation of some genes may be affected by various non-neoplastic factors. Such factors may include demographic variation, particularly age [14], exposures such as smoking [15], alcohol intake [15,16], or analgesic use [17], and body mass [18] or diabetes mellitus [19]. Furthermore, aberrant methylation on some genes has been detected in histologically normal mucosa at points distant from colorectal neoplasms [20] and such molecular field defects could conceivably contribute to non-specificity on stool testing.…”

mentioning

confidence: 99%

Aberrantly Methylated Gene Marker Levels in Stool: Effects of Demographic, Exposure, Body Mass, and Other Patient Characteristics

Ahlquist¹,

Taylor²,

Yab³

et al. 2012

J Mol Biomark Diagn

View full text Add to dashboard Cite

Introduction Stool DNA testing has emerged as a patient-friendly, noninvasive, and easily distributable new approach to colorectal cancer (CRC) screening that achieves high detection rates of both CRC and clinically significant precancerous lesions [1,2]. Incorporating key advances, including next generation analytical technology and broadly informative marker panels, prototype stool DNA tests in recent case-control studies have yielded sensitivities for curable stage CRC of 87-98% and for adenomas >1 cm of 64% and higher with increasing size at specificity cutoff ≥ 90% [3-5]. An understanding of factors that contribute to non-specificity is critical to optimizing test configuration and clinical use of this screening approach. Yet, relatively little has been reported about the effects of common clinical variables on stool DNA marker levels. This is particularly true of aberrantly methylated gene markers which, to date, have proven to be the most informative panel elements in prototype stool DNA tests [3-5]. Aberrant methylation of the promoter region of numerous genes occurs early during colorectal carcinogenesis [6-10]. While there exists remarkable molecular heterogeneity across colorectal neoplasms, we [3,10,11] and others [7,9,12,13] have found that several aberrantly methylated gene markers alone or in combination almost perfectly discriminate CRC and adenomas from normal colorectal mucosa at the tissue level. However, many of these candidate markers fail on stool application due to non-specificity resulting from high marker background levels [3,10]. In a recent large study [3], we selected four methylated gene markers (BMP3, NDRG4, vimentin, and TFPI2) that maintained both high sensitivity and high specificity for detection of CRC and advanced adenomas on stool testing. The effects of common clinical covariates on these 4 candidate methylation markers have not been evaluated. Based on observations across different tissues, rates of aberrant methylation of some genes may be affected by various non-neoplastic factors. Such factors may include demographic variation, particularly age [14], exposures such as smoking [15], alcohol intake [15,16], or analgesic use [17], and body mass [18] or diabetes mellitus [19]. Furthermore, aberrant methylation on some genes has been detected in histologically normal mucosa at points distant from colorectal neoplasms [20] and such molecular field defects could conceivably contribute to non-specificity on stool testing. Abstract Background: Selected aberrantly methylated genes represent sensitive candidate stool markers for colorectal cancer (CRC) screening. We assessed the impact of demographic, exposure, body mass, and other patient variables on stool levels of highly informative methylated gene markers-BMP3, NDRG4, vimentin, and TFPI2.

show abstract

Alcohol consumption in relation to aberrant DNA methylation in breast tumors

Cited by 29 publications

References 43 publications

Lifetime Alcohol Intake, Binge Drinking Behaviors, and Breast Cancer Risk

Lifetime Alcohol Intake, Binge Drinking Behaviors, and Breast Cancer Risk

Links between Alcohol Consumption and Breast Cancer: A Look at the Evidence

Aberrantly Methylated Gene Marker Levels in Stool: Effects of Demographic, Exposure, Body Mass, and Other Patient Characteristics

Contact Info

Product

Resources

About