Cancer screening of upper aerodigestive tract in Japanese alcoholics with reference to drinking and smoking habits and aldehyde dehydrogenase-2 genotype

Yokoyama, Akira; Ohmori, Tai; Muramatsu, Taro; Higuchi, Susumu; Yokoyama, Tetsuji; Matsushita, Satoru; Matsumoto, Morio; Maruyama, Katsuya; Hayashida, Motoi; Ishii, Hiromasa

doi:10.1002/(sici)1097-0215(19961104)68:3<313::aid-ijc8>3.0.co;2-4

Cited by 79 publications

(41 citation statements)

References 12 publications

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“…If more than one article was published from the same case series, we included the paper where the most individuals were reported in the analysis. Of the 31 articles retrieved, 12 studies were eligible for the meta-analysis (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22). Six reports (17)(18)(19)(20)(21)(22) were later excluded because they were subjects included in an expanded series (13).…”

Section: Methodsmentioning

confidence: 99%

“…Of the 31 articles retrieved, 12 studies were eligible for the meta-analysis (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22). Six reports (17)(18)(19)(20)(21)(22) were later excluded because they were subjects included in an expanded series (13). Finally, six case-control studies conducted on Japanese, and comprising a total of 945 cases and 2,917 controls were retained for the analysis (11)(12)(13)(14)(15)(16).…”

Section: Methodsmentioning

confidence: 99%

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Aldehyde Dehydrogenase 2 and Head and Neck Cancer: A Meta-analysis Implementing a Mendelian Randomization Approach

Boccia

Hashibe

Galli

et al. 2009

Cancer Epidemiology, Biomarkers &Amp; Prevention

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113

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Alcohol drinking at high doses is a risk factor for head and neck cancer, and exposure to acetaldehyde, the principle metabolite of alcohol, is supposed to account for the increased risk. Individuals homozygous for the *2 variant allele of aldehyde dehydrogenase 2 (ALDH2) are unable to metabolize acetaldehyde, which prevents them from alcohol drinking, whereas *1*2 have 6-fold higher blood acetaldehyde concentration postalcohol consumption with respect to *1*1. According to the concept of Mendelian randomization, because this polymorphism is distributed randomly during gamete formation, its association with head and neck cancer should be not confounded by smoking. We carried out a meta-analysis of ALDH2 and head and neck cancer searching for relevant studies on Medline and Embase up to January 31, 2008, and investigated the consistency between the expected odds ratio (OR) among drinkers from the largest pooled analysis among never smokers and the observed OR from this meta-analysis by an interaction test. Six studies were selected (945 cases, 2,917 controls). The OR of head and neck cancer among *2*2 was 0.53 [95% confidence interval (95% CI), 0.28-1.00] relative to *1*1 and 1.83 (95% CI, 1.21-2.77) among *1*2. The expected OR for head and neck cancer due to alcohol intake among *1*1 was 1.38 (95% CI, 0.88-2.17) and the observed OR among *1*1 compared with 2*2 from this meta-analysis was 1.88 (95% CI, 1.00-3.57; P for interaction = 0.43). Besides showing the effectiveness of the Mendelian randomization approach, these findings support the theory that alcohol increases head and neck cancer risk through the carcinogenic action of acetaldehyde. (Cancer Epidemiol Biomarkers Prev 2009;18(1):248-54)

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Aldehyde Dehydrogenase 2 and Head and Neck Cancer: A Meta-analysis Implementing a Mendelian Randomization Approach

Boccia

Hashibe

Galli

et al. 2009

Cancer Epidemiology, Biomarkers &Amp; Prevention

Self Cite

113

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“…19) The former is the wild-type with full enzyme activity and the latter is the mutant type with reduced activity. While those with the wild-type homozygote (ALDH2 Takeshita et al 21) reported that the mean amount of alcohol consumption in the ALDH2 * 22,23) demonstrated that the ALDH2 heterozygous individuals who regularly consume large amounts of alcohol belong to a high risk group. The statistical association of alcohol intake with the frequency of colon cancer, which has been demonstrated among Japanese, [14][15][16][17][18] might be influenced by this genotype difference.…”

Section: Abstract: Colorectal Cancer -Alcohol Drinking -Aldh2 Genotypementioning

confidence: 99%

Genotype Difference of Aldehyde Dehydrogenase 2 Gene in Alcohol Drinkers Influences the Incidence of Japanese Colorectal Cancer Patients

Murata

Tagawa

Watanabe

et al. 1999

Japanese Journal of Cancer Research

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A case-control study was conducted to explore the possible etiologic role of alcohol and aldehyde dehydrogenase 2 (ALDH2) gene among Japanese colorectal cancer patients. Information on their drinking, smoking and dietary habits was collected from 265 colon and 164 rectum cancer patients, and 794 non-cancer patients as a control group. Genotypes of the ALDH2 gene at codon 487, glutamic acid (ALDH2 * 1) as a wild-type or lysine (ALDH2 * 2) as a mutated type with reduced enzyme activity, were analyzed by polymerase chain reaction in 160 colon and 110 rectum cancer patients and 121 control persons. Univariate analysis with the χ χ χ χ 2 statistical test showed that heavy alcohol drinking (P < < < <0.01), frequent meat intake (P < < < <0.001), and irregular (P < < < <0.01), hasty (P < < < <0.01) and excessive (P < < < <0.001) eating habits were associated with the incidence of both colon and rectum cancers, whereas heavier smoking (P < < < <0.05) and infrequent fish (P < < < <0.03) and fruit (P < < < <0.01) intake were solely associated with incidence of rectum cancer. Infrequent green vegetable intake was not correlated with the incidence of colorectal cancer. Multivariate unconditional logistic regression analysis confirmed the association of alcohol consumption (P < < < <0.01) and meat intake (P < < < <0.05).Homozygous and heterozygous carriers of ALDH2 * 2 allele tended to be found in colon (trend P = = = =0.04) but not in rectum cancer patients compared to controls. Risk elevation for colon cancer due to alcohol consumption was pronounced among the heterozygotes and it was statistically significant especially for distal colon cancer (trend P = = = =0.02). We conclude that alcohol consumption is a risk factor for colorectal cancer and the risk can be enhanced in ALDH2 heterozygotes.

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“…25 Excessive alcohol consumption among smokers has been associated with an elevated risk of esophageal cancer. 26,27 X-ray repair cross-complementing 1 (XRCC1) is a major gene in the DNA base excision repair (BER) pathway. A polymorphism of XRCC1 arginine (Arg)399 glutamine (Gln) has been associated with altered DNA repair capacity and cancer risk.…”

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confidence: 99%

Dietary selenium intake, aldehyde dehydrogenase‐2 and X‐ray repair cross‐complementing 1 genetic polymorphisms, and the risk of esophageal squamous cell carcinoma

Cai

You

et al. 2006

Cancer

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BACKGROUND.To the authors' knowledge, few studies have been conducted to date regarding dietary selenium and the potential gene-nutrient interactions with single-nucleotide polymorphisms (SNPs) in different pathways on the risk of esophageal cancer. METHODS. The authors investigated the role of dietary selenium intake and itsinterplay with SNPs of the ALDH2 (glutamic acid [Glu] 487 lysine [Lys]) and the X-ray repair cross-complementing 1 (XRCC1) (arginine [Arg] 399 glutamine [Gln]) genes on the risk of esophageal squamous cell carcinoma (ESCC) in a populationbased, case-control study in China. In total, 218 patients with ESCC and 415 healthy population control participants were interviewed. Dietary selenium intake was estimated from a food frequency questionnaire with 97 food items. ALDH2 and XRCC1 polymorphisms were detected with a polymerase chain reaction-restriction fragment length polymorphism assay. RESULTS.The adjusted odds ratio (OR) for the highest quintile of dietary selenium intake, compared with the lowest quintile of intake, was 0.48 (95% confidence interval [95% CI], 0.25-0.89), with a strong dose-response relation (P for trend, Ͻ.01). The ALDH2 Lys and XRCC1 Gln variant alleles were associated with an increased risk of ESCC with adjusted ORs of 1.91 (95% CI, 0.96-3.80) and 1.67 (95% CI, 1.08-2.59), respectively. An elevation of the risk for ESCC was pronounced most among carriers of ALDH2 Lys/Lys and XRCC1 399Gln/Gln or Gln/Arg who consumed a low level of dietary selenium (adjusted OR, 4.16; 95% CI, 1.14-15.12). CONCLUSIONS.To the authors' knowledge, this is the first in-depth study to suggest that genetic susceptibility may modify the association between selenium intake and the risk of ESCC. The findings indicated that individuals with low dietary selenium intake and ALDH2 Lys/Lys and XRCC1 399Gln/Gln or Gln/Arg genotypes were associated with an increased ESCC risk, especially in the presence of exposure to tobacco and alcohol carcinogens. A ccumulating evidence from prior epidemiologic studies suggests an association between esophageal cancer and the use of alcohol and tobacco. [1][2][3] The combined use of alcohol and tobacco leads to synergistically increased risk of esophageal cancers. 4,5 In Europe and North America, it is believed that 90% of esophageal cancers are related to tobacco smoking and alcohol drinking. Simultaneous exposure to similarly moderate amounts of smoking and alcohol drinking increased the risk 12-fold and 19-fold in men and women, respectively. 6 Engel et al., in a multicenter, population-based, case-control study, observed that ever-smoking and alcohol consumption accounted for 56.9% and 72.4% of esophageal squamous cell carcinoma (ESCC) in men and women, respectively. 7 Diet has been implicated in many pathways involved in carcinogenesis, including DNA repair and carcinogen metabolism. In addition to myriad phytochemicals, diet provides numerous trace minerals that are essential for normal metabolism, including selenium, which is suggested as a potential chemopreven...

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Cancer screening of upper aerodigestive tract in Japanese alcoholics with reference to drinking and smoking habits and aldehyde dehydrogenase-2 genotype

Cited by 79 publications

References 12 publications

Aldehyde Dehydrogenase 2 and Head and Neck Cancer: A Meta-analysis Implementing a Mendelian Randomization Approach

Aldehyde Dehydrogenase 2 and Head and Neck Cancer: A Meta-analysis Implementing a Mendelian Randomization Approach

Genotype Difference of Aldehyde Dehydrogenase 2 Gene in Alcohol Drinkers Influences the Incidence of Japanese Colorectal Cancer Patients

Dietary selenium intake, aldehyde dehydrogenase‐2 and X‐ray repair cross‐complementing 1 genetic polymorphisms, and the risk of esophageal squamous cell carcinoma

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