Alcohol consumption, variability in alcohol dehydrogenase genes and risk of renal cell carcinoma

Antwi, Samuel O.; Eckel‐Passow, Jeanette E.; Diehl, Nancy; Serie, Daniel J.; Custer, Kaitlynn; Wu, Kevin J.; Cheville, John C.; Thiel, David D.; Leibovich, Bradley C.; Parker, Alexander S.

doi:10.1002/ijc.31103

Cited by 14 publications

(14 citation statements)

References 50 publications

(150 reference statements)

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“…In the current study, even light to moderate levels of lifetime alcohol consumption appeared to increase most of the upper aerodigestive and gastrointestinal cancers . In contrast to the patterns observed in Western settings, we observed no protective effects of light to moderate lifetime alcohol consumption for colorectal and kidney cancers. For breast and prostate cancer, different pathways such as elevations of circulating sex hormone levels (ie, estrogens and androgens) by alcohol use may explain the alcohol‐related cancer risk at even light to moderate levels of lifetime alcohol consumption .…”

Section: Discussioncontrasting

confidence: 99%

“…Drinking alcohol is a contributor to the overall cancer burden. In Western settings, alcohol‐related cancer risk has been characterized as a J‐shape pattern in some instances (colorectal and kidney cancers), and this suggests potential protective effects of alcohol . However, in 2018, the American Society of Clinical Oncology stated that more than 5% of new cancer cases were attributable to alcohol consumption .…”

Section: Introductionmentioning

confidence: 99%

“…In Western settings, alcohol-related cancer risk has been characterized as a J-shape pattern in some instances (colorectal and kidney cancers), and this suggests potential protective effects of alcohol. [1][2][3] However, in 2018, the American Society of Clinical Oncology stated that more than 5% of new cancer cases were attributable to alcohol consumption. 4 Upper aerodigestive tract (oral, laryngeal, and esophageal), colorectal, and liver cancers represented 60%, 21%, and 13% of alcohol-related cancer cases in men, respectively, whereas breast, upper aerodigestive tract, liver, and colorectal cancers represented 52%, 25%, 12%, and 6% of alcohol-related cancer cases in women, respectively.…”

Section: Introductionmentioning

confidence: 99%

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Light to moderate amount of lifetime alcohol consumption and risk of cancer in Japan

Zaitsu

Takeuchi

Kobayashi

et al. 2019

Cancer

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Background Even light to moderate alcohol consumption has been shown to increase cancer incidence. However, this association has not been well characterized in Japan. Methods Based on a nationwide, hospital‐based data set (2005‐2016), a multicenter case‐control study was conducted (63,232 cancer cases and 63,232 controls matched for sex, age, admission date, and admitting hospital). The total amount of lifetime alcohol consumption (drink‐years) was recalled for each patient by multiplication of the daily amount of standardized alcohol use (drinks per day) and the duration of drinking (years). Odds ratios (ORs) were estimated for overall and specific cancer sites via conditional logistic regression with restricted cubic splines, with adjustments made for smoking, occupational class, and comorbidities. Lifetime abstainers served as the reference group. Results Spline curves showed a dose‐response association with overall cancer risk: the minimum risk was at 0 drink‐years, and the OR at 10 drink‐years was 1.05 (95% confidence interval [CI], 1.04‐1.06). In comparison with lifetime abstainers, the OR for >0 to 20 drink‐years was 1.06 (95% CI, 1.01‐1.11). Those who drank 2 drinks or fewer per day had elevated odds for overall cancer risk across all duration‐of‐drinking categories. The same patterns were observed at light to moderate levels of drinking for most gastrointestinal/aerodigestive cancers as well as breast and prostate cancers. Analyses stratified by sex, different drinking/smoking behaviors, and occupational class mostly showed the same patterns for overall cancer incidence associated with light to moderate levels of drinking. Conclusions In Japan, even light to moderate alcohol consumption appears to be associated with elevated cancer risks.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Light to moderate amount of lifetime alcohol consumption and risk of cancer in Japan

Zaitsu

Takeuchi

Kobayashi

et al. 2019

Cancer

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“…As known, alcohol tolerance varies greatly from person to person, and some nations consume more alcohol than others. Although studies on individual differences in alcohol consumption and CKD are limited, existing studies have found that individual variation in an alcohol dehydrogenase gene may play a role [98], but more studies are needed to confirm these findings.…”

Section: Association Between Alcohol Consumption and Chronic Kidney Dmentioning

confidence: 99%

Alcohol Consumption Can be a “Double-Edged Sword” for Chronic Kidney Disease Patients

Fan

Yun

et al. 2019

Med Sci Monit

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Excessive drinking of alcohol is becoming a worldwide problem, and people have recognized that there exists a close relationship between chronic kidney disease (CKD) and alcohol consumption. However, there are many inconsistencies between experimental and clinical studies on alcohol consumption and kidney damage. The possible reason for this contradictory conclusion is the complex drinking pattern of humans and some bioactivators in wine. In addition, the design itself of the clinical studies can also produce conflicting interpretations of the results. Considering the benefits of light-to-moderate alcohol consumption, we recommend that CKD patients continue light-to-moderate drinking, which is beneficial to them. Because alcohol consumption can lead to adverse events, we do not advise non-drinkers to start to drink. Although light-to-moderate alcohol consumption may not pose a risk to patients with CKD, the patients’ condition needs to be considered. Consumption of even small amounts of alcohol can be associated with increased death risk. Additional clinical and experimental studies are needed to clarify the effect of alcohol on the kidneys and alcohol consumption on CKD patients.

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“…Multiple studies have assessed gene-environment interactions in RCC and ccRCC. RCC risk has been found to be associated with interactions between alcohol consumption and ADH7 26 ; sodium and hypertension and AGTR, AGT and ACE 31 ; calcium and vitamin D intake and RXRA 28 ; tobacco smoking and NAT2, CYP1A1 and GSTM1 25 ; and meat-cooking mutagens and ITPR2 and EPAS1 27 . To our knowledge, we are the first to study gene-environment interactions between the selected VHL and HIF1A SNPs and smoking, hypertension, BMI and alcohol consumption.…”

Section: Discussionmentioning

confidence: 99%

Germline polymorphisms in the Von Hippel-Lindau and Hypoxia-inducible factor 1-alpha genes, gene-environment and gene-gene interactions and renal cell cancer

Pol

Brandt

Engeland

et al. 2020

Sci Rep

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We investigated the relationship between germline single nucleotide polymorphisms (Snps) in Von Hippel-Lindau (VHL) and Hypoxia-inducible factor 1-alpha (HIF1A), and their gene-environment and gene-gene interactions, and clear-cell Rcc (ccRcc) risk. furthermore, we assessed the relationship between VHL Snps and VHL promoter methylation. three VHL polymorphisms and one HIF1A polymorphism were genotyped in the Netherlands Cohort Study. In 1986, 120,852 participants aged 55-69 completed a self-administered questionnaire on diet and lifestyle and toenail clippings were collected. Toenail DNA was genotyped using the Sequenom MassARRAY platform. After 20.3 years, 3004 subcohort members and 406 RCC cases, of which 263 ccRCC cases, were eligible for multivariate case-cohort analyses. VHL_rs779805 was associated with RCC (Hazard Ratio (HR) 1.53; 95% Confidence Interval (CI) 1.07-2.17) and ccRCC risk (HR 1.88; 95% CI 1.25-2.81). No associations were found for other SNPs. Potential gene-environment interactions were found between alcohol consumption and selected SNPs. However, none remained statistically significant after multiple comparison correction. no gene-gene interactions were observed between VHL and HIF1A. VHL promoter methylation was not associated with VHL Snps. VHL SNPs may increase (cc)RCC susceptibility. No associations were found between gene-environment and gene-gene interactions and (cc)Rcc risk and between VHL promoter methylation and VHL Snps. Genetic and epigenetic alterations in the Von Hippel-Lindau (VHL) gene are important drivers of carcinogenesis in clear-cell renal cell carcinoma (ccRCC) 1. For sporadic ccRCC, biallelic inactivation of VHL because of rare, but highly penetrant, somatic mutations is relatively common 2,3. Previous studies have estimated that 50-82% of patients with sporadic ccRCC have a mutation in the VHL gene 4-8. The VHL gene encodes the VHL tumor suppressor protein (pVHL). Inactivation of pVHL leads to the unchecked accumulation of hypoxia-inducible factor 1 alpha (HIF1A), which facilitates oxygen delivery, adaptation to oxygen deprivation and angiogenesis 1,9. Therefore, genetic or epigenetic alterations in VHL and HIF1A may lead to enhanced cell survival and carcinogenesis. In contrast to the rare, but highly penetrant, sequence alterations leading to VHL loss, some germline Single Nucleotide Polymorphisms (SNPs) are highly frequent, but have a low penetrance. In general, SNPs account for many different phenotypes as they may alter disease susceptibility by affecting the gene's function 10. Genome-wide

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Alcohol consumption, variability in alcohol dehydrogenase genes and risk of renal cell carcinoma

Cited by 14 publications

References 50 publications

Light to moderate amount of lifetime alcohol consumption and risk of cancer in Japan

Light to moderate amount of lifetime alcohol consumption and risk of cancer in Japan

Alcohol Consumption Can be a “Double-Edged Sword” for Chronic Kidney Disease Patients

Germline polymorphisms in the Von Hippel-Lindau and Hypoxia-inducible factor 1-alpha genes, gene-environment and gene-gene interactions and renal cell cancer

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