Evidence for an Important Role of Alcohol- and Aldehyde-Metabolizing Genes in Cancers of the Upper Aerodigestive Tract

Hashibe, Mia; Boffetta, Paolo; Заридзе, Давид; Shangina, Oxana; Szeszenia-Da̧browska, Neonila; Mateș, Dana; Janout, Vladimí­r; Fabiánovà, Eleonóra; Bencko, Vladimír; Moullan, Norman; Chabrier, Amélie; Hung, Rayjean J.; Hall, Janet; Canzian, Federico; Brennan, Paul

doi:10.1158/1055-9965.epi-05-0710

Cited by 166 publications

(135 citation statements)

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“…However, further analyses in the rs1573496 (ADH7) polymorphism showed that alcohol intake was associated with CRC risk among heterozygous and homozygous carriers of the rare rs1573496(C) (ADH7) allele, while among homozygous wild-type participants the alcohol CRC association was weak. With respect to SNPs in the ALDH family, similar genes alcohol interactions have been previously observed for upper aero-digestive tract cancer, 21 for head and neck cancer, 31 and for CRC. 15 The alleles encoding the different ADH variants are heterogeneously distributed among ethnic groups.…”

Section: Discussionsupporting

confidence: 72%

“…33 For alcohol-related cancers, an increased risk of upper aero-digestive tract cancers has been observed consistently in studies conducted in Europe 21,34 and in Japan. 35 For CRC, no clear explanation for the increased risk associated with the slow alcohol metabolizer rs1229984(G) (ADH1B) allele observed in Asian populations 15,16 has been provided.…”

Section: Discussionmentioning

confidence: 79%

“…21 Genotyping for rs1229984 (ADH1B), rs1573496 (ADH7) and rs441 (ALDH2) polymorphisms was performed by Taqman methodology in 384-well plates read with the Sequence Detection Software on an ABI-Prism7900 instrument, according to the manufacturer's instructions (Applied Biosystems / Life Technologies, Saint-Aubin, France). Primers and probes were supplied by Applied Biosystems (Assays-by-Design).…”

Section: Snp Selection/genotyping and Folate Assessmentmentioning

confidence: 99%

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Alcohol dehydrogenase and aldehyde dehydrogenase gene polymorphisms, alcohol intake and the risk of colorectal cancer in the European Prospective Investigation into Cancer and Nutrition study

et al. 2012

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BACKGROUND/OBJECTIVES:Heavy alcohol drinking is a risk factor of colorectal cancer (CRC), but little is known on the effect of polymorphisms in the alcohol-metabolizing enzymes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) on the alcohol-related risk of CRC in Caucasian populations. SUBJECTS/METHODS: A nested case-control study (1269 cases matched to 2107controls by sex, age, study centre and date of blood collection) was conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC) to evaluate the impact of rs1229984 (ADH1B), rs1573496 (ADH7) and rs441 (ALDH2) polymorphisms on CRC risk. Using the wild-type variant of each polymorphism as reference category, CRC risk estimates were calculated using conditional logistic regression, with adjustment for matching factors. RESULTS: Individuals carrying one copy of the rs1229984(A) (ADH1B) allele (fast metabolizers) showed an average daily alcohol intake of 4.3 g per day lower than subjects with two copies of the rs1229984(G) allele (slow metabolizers) (P diff o0.01). None of the polymorphisms was associated with risk of CRC or cancers of the colon or rectum. Heavy alcohol intake was more strongly associated with CRC risk among carriers of the rs1573496(C) allele, with odds ratio equal to 2.13 (95% confidence interval: 1.26-3.59) compared with wild-type subjects with low alcohol consumption (P interaction ¼ 0.07). CONCLUSIONS: The rs1229984(A) (ADH1B) allele was associated with a reduction in alcohol consumption. The rs1229984 (ADH1B), rs1573496 (ADH7) and rs441 (ALDH2) polymorphisms were not associated with CRC risk overall in Western-European populations. However, the relationship between alcohol and CRC risk might be modulated by the rs1573496 (ADH7) polymorphism.

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 79%

Section: Snp Selection/genotyping and Folate Assessmentmentioning

confidence: 99%

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Alcohol dehydrogenase and aldehyde dehydrogenase gene polymorphisms, alcohol intake and the risk of colorectal cancer in the European Prospective Investigation into Cancer and Nutrition study

et al. 2012

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“…17 1 1 0 0 1 1 1 0 1 0 Cui et al 18 1 1 1 0 1 1 1 0 1 1 Dikshit and Kanhere 19 1 0 1 0 1 1 1 0 1 1 Elahi et al 20 1 1 1 0 1 1 1 1 1 1 Elwood et al 21 1 1 0 0 1 1 1 0 1 1 Franceschi et al 22 1 1 0 0 1 1 1 1 1 0 Franceschi et al 23 1 0 0 0 1 1 0 1 1 1 Franco et al 24 1 1 0 0 1 1 1 0 1 0 Greenberg et al 25 0 0 1 0 1 1 1 1 1 1 Guneri et al 26 0 1 0 0 1 1 0 0 1 0 Hashibe et al 27 1 1 0 0 1 1 1 0 1 1 Hayes et al 28 1 1 1 0 1 1 1 1 1 1 Herrero et al 29 1 1 0 0 1 1 1 1 1 1 Kabat et al 30 0 1 0 0 1 1 1 0 1 0 Ko et al 31 1 0 0 0 1 1 1 0 1 0 Levi et al 32 0 0 0 0 1 1 1 1 1 1 Llewellyn et al 33 1 1 1 0 1 1 1 0 1 0 Llewellyn et al 34 1 1 1 0 1 1 1 1 1 0 Lu et al 35 0 1 1 0 1 1 1 0 0 0 Maden et al 36 1 0 1 0 1 1 1 0 1 1 Marshall et al 37 0 1 1 0 1 1 1 0 1 0 Mashberg et al 38 0 1 0 0 1 1 1 0 1 1 Merchant et al 39 0 1 0 1 1 1 1 0 1 0 Merletti et al 40 1 1 1 0 1 1 1 0 1 0 Moreno-Lopez et al 41 1 1 1 0 1 1 0 0 1 0 Muscat et al 42 1 1 0 0 1 1 1 1 1 1 Nandakumar et al 43 1 1 0 0 1 1 1 0 1 0 Olshan et al 44 1 1 0 0 1 1 1 1 1 1 Pacella-Norman 45 1 1 0 0 1 1 1 0 1 1 Rao et al 46 1 0 0 0 1 1 1 0 1 1 Rogers et al 47 1 0 1 0 1 1 1 1 1 0 Rosenquist 48 1 1 1 0 1 1 1 1 1 0 Schwartz et al 49 1 1 1 0 1 1 1 0 1 1 Smith et al 50 1 1 0 0 1 1 1 0 1 0 Toporcov et al 51 1 53 1 1 0 1 1 0 1 0 1 1 Zheng et al 54 1 1 0 0 1 1 1 1 1 1 Znaor et al 55 1 0 0 0 1 1 0 1 1 0 A: Expli...…”

Section: Study Characteristicsmentioning

confidence: 99%

Socioeconomic inequalities and oral cancer risk: A systematic review and meta‐analysis of case‐control studies

Conway

Petticrew

Marlborough³

et al. 2008

Intl Journal of Cancer

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221

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There is uncertainty and limited recognition of the relationship between socioeconomic inequalities and oral cancer. We aimed to quantitatively assess the association between socioeconomic status (SES) and oral cancer incidence risk. A systematic review of casecontrol studies obtained published and unpublished estimates of the SES risk related to oral cancer. Studies were included which reported odds ratios (ORs) and corresponding 95% CIs of oral cancer with respect to SES, or if the estimates could be calculated or obtained. Meta-analyses were performed on subgroups: SES measure, age, sex, global region, development level, time-period and lifestyle factor adjustments; while sensitivity analyses were conducted based on study methodological issues. Forty-one studies provided 15,344 cases and 33,852 controls which met our inclusion criteria. Compared with individuals who were in high SES strata, the pooled ORs for the risk of developing oral cancer were 1.85 (95%CI 1.60, 2.15; n 5 37 studies) for those with low educational attainment; 1.84 (1.47, 2.31; n 5 14) for those with low occupational social class; and 2.41 (1.59, 3.65; n 5 5) for those with low income. Subgroup analyses showed that low SES was significantly associated with increased oral cancer risk in high and lower income-countries, across the world, and remained when adjusting for potential behavioural confounders. Inequalities persist but are perhaps reducing over recent decades. Oral cancer risk associated with low SES is significant and comparable to lifestyle risk factors. Our results provide evidence to steer health policy which focus on lifestyles factors toward an integrated approach incorporating measures designed to tackle the root causes of disadvantage. ' 2008 Wiley-Liss, Inc.Key words: meta-analysis; oral cancer; SES; socioeconomic status; systematic review In 2000, oral cancer (ICD-10 C00-06) was estimated to be the 8th most common cancer worldwide-with an estimated 267,000 new cases and 128,000 deaths, and with the greatest burden in developing countries. 1 Despite a wealth of literature on the effects of poverty and inequality on health, 2 the effect of socioeconomic circumstances on oral cancer is given little recognition in a predominant medical model approach to research and prevention on the risks of the disease. 3 Recent published work on the relationship between socioeconomic status (SES) and oral cancer has mainly been in the form of descriptive epidemiology studies linking routine registry data to census data. From such studies, increased risk of oral cancer appears associated with high levels of area-based socioeconomic deprivation, 4,5 although this was not reflected in a review of incidence studies from across the world which utilised mainly individual measures of SES. 6 Area-based measures are liable to the 'ecological fallacyÕ whereby individuals are allocated SES based on their area of residence. The few analytical studies to focus on SES have also been equivocal, and socioeconomic correlates have recently been found to be c...

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“…11,16 Studies in several populations have found that the risk of esophageal SCC (ESCC) is closely associated with genetic polymorphisms of the two alcohol-metabolizing genes, and this relationship has been suggested to be alcohol amount dependent. [17][18][19] Recently, the mutant ALDH2 Glu487Lys allele in molecular epidemiological studies has been reported to be more prevalent among head and neck carcinoma (HNC) patients of a younger diagnosed age (<66 years). 20 Earlier multiple esophageal dysplasias in HNC patients have also been linked to the presence of this variant allele.…”

Section: Uiccmentioning

confidence: 99%

Genetic modulation of ADH1B and ALDH2 polymorphisms with regard to alcohol and tobacco consumption for younger aged esophageal squamous cell carcinoma diagnosis

Lee¹,

Wu²,

Wu³

et al. 2009

Intl Journal of Cancer

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Genetic variants in alcohol dehydrogenase-1B (ADH1B) and aldehyde dehydrogenase-2 (ALDH2) genes modulate acetaldehyde removal upon alcohol ingestion. Although these genetic vulnerabilities have been linked to higher esophageal squamous cell carcinoma (ESCC) risks, it is unclear whether they also determine the time of malignancy presentation. The purpose of this investigation was to unravel genotoxic effects of the two alcohol-metabolizing genes with regard to alcohol and tobacco consumption on the age at ESCC diagnosis and tumor dissemination. ADH1B/ALDH2 genotyping was performed on lymphocyte DNA specimens taken from 406 consecutively registered incident patients with pathology-proven ESCC. To fully utilize individual genetic and survival information, survival analyses and gene-longevity applied approaches were introduced. Among heavy drinkers, the ADH1B Arg/Arg (55 years) and ALDH2 Glu/Lys genotypes (54 years) were found to confer a 15 and 16 years earlier carcinoma diagnosed age than His/His and Glu/Glu nondrinkers (both 70 years), respectively. For drinkers, 1-year age advancement was, separately, associated with a 0.977 and 0.953-fold stepwise reduced likelihood of being ADH1B Arg homozygote and ALDH2 Lys variant. Noticeably elevated hazard-ratio (HR) for drinkers of ADH1B slow-form genotype and ALDH2 inactive-form allele were identified in smokers (HR 5 2.3-2.6), but no in nonsmokers. In smokers, appreciably higher cumulative cancer onset risks were correspondingly recognized from the age of 45 and 49 upward among any 1 Lys allele and Arg/Arg 1 Glu/Glu combined-ADH1B/ALDH2-genotype drinkers than nondrinkers. In conclusion, consumption of tobacco and alcohol, coupled with genetic susceptibilities associated with acetaldehyde elimination, as modulated by ADH1B and ALDH2 genotypes, determines a substantial magnitude of tumorigenetic effect on earlier age ESCC diagnosis. ' 2009 UICC Key words: age factor; alcohol drinking; alcohol dehydrogenase; aldehyde dehydrogenase; areca; esophageal neoplasms; smoking Carcinoma stemming from the esophagus ranks as the eighth most common cancer in the world and is one of the deadliest and, yet, most neglected forms of cancer.1 Given the insidious nature of this neoplasm, it has been found that more than 50% of the eventual patients already have unresectable and/or metastatic conditions at the time of tumor presentation.2 Although recent advances in the diagnosis, staging and treatment of esophageal cancer have brought about noteworthy improvement toward some manner of survival, 75% of the patients still die within 1 year of diagnosis, and currently just 5-14% of such patients survive at least 5 years.2,3 Due, in part, to the high case fatality rate, younger esophageal carcinoma onset has been linked to a shorter life expectancy. This leads to a number of challenging health-related issues for the respective family, as well as to substantial work productivity losses for the country.Alcohol intake is a well-recognized determinant for squamous cell carcinoma (SCC) of the esopha...

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Evidence for an Important Role of Alcohol- and Aldehyde-Metabolizing Genes in Cancers of the Upper Aerodigestive Tract

Cited by 166 publications

References 30 publications

Alcohol dehydrogenase and aldehyde dehydrogenase gene polymorphisms, alcohol intake and the risk of colorectal cancer in the European Prospective Investigation into Cancer and Nutrition study

Alcohol dehydrogenase and aldehyde dehydrogenase gene polymorphisms, alcohol intake and the risk of colorectal cancer in the European Prospective Investigation into Cancer and Nutrition study

Socioeconomic inequalities and oral cancer risk: A systematic review and meta‐analysis of case‐control studies

Genetic modulation of ADH1B and ALDH2 polymorphisms with regard to alcohol and tobacco consumption for younger aged esophageal squamous cell carcinoma diagnosis

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