Alcohol and Cancer: Mechanisms and Therapies

Ratna, Anuradha; Mandrekar, Pranoti

doi:10.3390/biom7030061

Cited by 109 publications

(110 citation statements)

References 156 publications

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“…A loss of retinoic acid has a negative effect on cell differentiation and thus enhances carcinogenesis [30]. Moreover, ethanol increases cellular membrane permeability and acts as a solvent to facilitate penetration of (pro-)carcinogens into the intracellular domain of mucosal epithelial cells [5,14,15]. High-risk alcohol drinkers who smoke should be advised to quit alcohol and tobacco and should consider going for a screening oesophagogastroduodenoscopy.…”

Section: Oesophageal Cancermentioning

confidence: 99%

“…The main component of alcoholic drinks is ethanol. Once ingested, alcohol (ethanol) is metabolized by alcohol dehydrogenase (ADH) into acetaldehyde, which by aldehyde dehydrogenase (ALDH) is then oxidized to acetate [14,15].…”

Section: Introductionmentioning

confidence: 99%

“…Acetaldehyde exerts permanent damage on DNA strands, inhibits DNA repair mechanisms, and shortens telomere length [14][15][16]. Alcohol promotes ROS generation and impairs the function of scavenger systems, thereby promoting oxidative stress and contributing to genetic instability [14][15][16]. The microbiome plays an important role as a link between alcohol use and gastrointestinal carcinogenesis [3,14,15].…”

Section: Introductionmentioning

confidence: 99%

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Alcohol Use and Gastrointestinal Cancer Risk

Scherübl¹

2020

Visc Med

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Background: Alcohol use is an important and potentially modifiable risk factor for gastrointestinal cancers. The more and the longer a person drinks, the higher the risk of cancer becomes. Even modest use of alcohol may increase cancer risk; 100 g of alcohol per week or less is currently considered to be the limit of low-risk use. Gastrointestinal Cancer Risk: Alcohol is causally associated with oesophageal squamous cell cancer, gastric cancer, hepatocellular carcinoma, colorectal cancer, and most likely also with pancreatic cancer. Alcohol when combined with tobacco smoking or excess body weight can act synergistically to cause gastrointestinal cancer. Exposure to alcohol may have contributed to the recent incidence increases of early-onset gastrointestinal cancers in some Western countries. Conclusions: People with longterm risky alcohol use should be encouraged to join cancer screening programmes. Alcohol cessation appears to be effective in reducing the alcohol-induced, increased cancer risk.

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Section: Oesophageal Cancermentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Alcohol Use and Gastrointestinal Cancer Risk

Scherübl¹

2020

Visc Med

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“…The liver is the most affected organ, since ethanol is mostly metabolized there [11,13], but gastrointestinal, central, and peripheral nervous systems; the heart and vascular system; endocrinological systems; nutrition; and musculo-skeletal systems are clearly affected [10]. In addition, ethanol is an immunosuppressive drug that is pro-inflammatory and pro-oncogenic [14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Fernández‐Solà

2020

Nutrients

105

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Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.

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“…Surely, even though mechanisms underlying alcohol-related carcinogenesis are not completely elucidated, different studies showed that chronic alcohol consumption, especially for high doses, could cause the onset of cancers(45)(46)(47).The mechanisms of alcohol on tumorigenesis include the production of acetaldehyde (derived from ethanol metabolism), oxidative stress, effects on metabolism, endocrine and immunity system, together with the influence of genetic polymorphisms regulating the absorption and the metabolic pathway of this substance (45-47). A multitude of genes contribute to the correct metabolism of alcohol, like those for ADH, ADLH, CYP2E1, and methylene-tetrahydrofolate reductase (MTHFR).…”

mentioning

confidence: 99%

Light alcohol drinking and the risk of developing cancer, a systematic review.

Ciardiello

Caprio

Picascia

et al. 2019

Preprint

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Background: There is strong evidence that heavy alcohol consumption (>50g per day) is a risk factor for several disease, including cancer. However, the oncogenic role of light alcohol drinking (<12,5g per day) is still controversial. The purpose of this review is to assess whether the intake of a single daily dose of alcohol could determine an increased risk of malignancy onset. Methods: A systemic PubMed research of meta-analysis studies, using the keywords “light alcohol drinking”, “light alcohol consumption” and “cancer”, was done. We established a period of 15 years, in order to select the most recent evidences; exclusively meta-analysis that specified levels of alcohol intake were included in the review. Studies focused on biochemical, molecular and genetic aspects, as well as duplicate articles were excluded. Results: We included in this review 29 large meta-analysis; light alcohol drinking was not associated with an increased risk of occurrence of most cancers, with the exception of breast, prostate cancer and, with less evidence, melanoma. Furthermore, a protective role of alcohol assumption on the development of bladder, kidney ovarian cancer and Non Hodgkin Lymphoma (NHL), has been described.Conclusions: We found that light alcohol drinking do not determine a higher risk for the insurgence of several malignancies, except for a light increase in the incidence of melanoma, breast cancer in women and prostate cancer in men.

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Alcohol and Cancer: Mechanisms and Therapies

Cited by 109 publications

References 156 publications

Alcohol Use and Gastrointestinal Cancer Risk

Alcohol Use and Gastrointestinal Cancer Risk

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Light alcohol drinking and the risk of developing cancer, a systematic review.

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