Abstract
Alcohol consumption has been established to be a major factor in the development and progress of cancer. Genetic polymorphisms of alcohol-metabolism genes result in differences between individuals in exposure to acetaldehyde, leading to possible carcinogenic effects. Arg47His (rs1229984 G > A) in ADH1B have been frequently studied for its potential effect on carcinogenesis. However, the findings are as yet inconclusive. To gain a more precise estimate of this potential association, we conducted a meta-analysis including 66 studies from 64 articles with 31999 cases and 50964 controls. The pooled results indicated that ADH1B Arg47His polymorphism is significantly associated with the decreased risk of overall cancer (homozygous model, odds ratio (OR) = 0.62, 95% confidence interval (CI) = 0.49–0.77; heterozygous model, OR = 0.71, 95% CI = 0.60–0.84; recessive model, OR = 0.83, 95% CI = 0.76–0.91; dominant model, OR = 0.62, 95% CI = 0.53–0.72; and allele comparison, OR = 0.82, 95% CI = 0.75–0.89). Stratified analysis by cancer type and ethnicity showed that a decreased risk was associated with esophageal cancer and head and neck cancer amongst Asians. In conclusion, our meta-analysis suggested that ADH1B Arg47His polymorphism was significantly associated with decreased overall cancer risk. These findings need further validation in large multicenter investigations.
Highlights
Received: 22 October 2018Revised: 03 March 2019Accepted: 08 March 2019Accepted Manuscript Online: Version of Record published: Cancer is a major public health problem worldwide
64 articles investigating the association between ADH1B Arg47His polymorphism and cancer risk were included in the final meta-analysis [17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80]
We found that ADH1B Arg47His polymorphism significantly associated with the decreased risk of overall cancer under all the five genetic models: homozygous model, odds ratio (OR) = 0.62, 95% confidence interval (CI) = 0.49–0.77; heterozygous
Summary
Received: 22 October 2018Revised: 03 March 2019Accepted: 08 March 2019Accepted Manuscript Online: Version of Record published: Cancer is a major public health problem worldwide. The incidence of cancer is predicted to reach 25 million worldwide by 2032 [2]. This growing cancer burden is expected as populations expand and age. Certain lifestyles, such as alcohol consumption, are likely to further boost the burden [1,2,3]. Acetaldehyde may stimulate carcinogenesis by disrupting DNA synthesis and repair, inhibiting DNA methylation, and by interacting with retinoid metabolism [8,9]. Genetic polymorphisms of alcohol-metabolism genes result in differences between individuals in exposure to acetaldehyde, leading to possible carcinogenic effects [10]. Compared with the Arg/Arg individuals, the His/His individuals have a 40-fold higher enzyme activity oxidized alcohol to toxic acetaldehyde [7]
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