Evidence map›Paper›PMID 42415227›Full record

ArticleCancer medicine2026

History of Alcohol-Related Cancers and ADH1B/ALDH2 Genotypes in a Large Japanese Cohort of Male Patients With Alcohol Dependence.

Akira Yokoyama, Tetsuji Yokoyama

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Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

2 authors.

Akira YokoyamaNational Hospital Organization Kurihama Medical and Addiction Center, Yokosuka, Japan.ORCID https://orcid.org/0000-0003-1869-1359
Tetsuji YokoyamaDepartment of Health Promotion, National Institute of Public Health, Wako, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlcohol-dependent (AD) patients frequently present with a history of alcohol-related cancers, but the timing of cancer treatment relative to the onset of advanced alcohol use disorder and the role of ADH1B/ALDH2 genotypes remain unclear.

methodsWe reviewed cancer histories at the initial visit of 5214 Japanese male AD patients (mean age 53.3 [SD 11.9] years), all genotyped for ADH1B (rs1229984) and ALDH2 (rs671). Multiple logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) for site-specific cancers, using fast-metabolizing ADH1B*2 and active ALDH2*1/*1 as the reference.

resultsAlcohol-related cancers were reported in 385 patients (7.38%): head and neck cancer (HNC) 1.05%, esophageal cancer (EC) 1.40%, gastric cancer (GC) 3.91%, colorectal cancer (CRC) 1.53%, and liver cancer (LC) 0.59%. Surgical treatment rates were high across sites. Most cancers were treated during or after the onset of advanced alcohol use disorder (HNC 81.8%, EC 74.0%, GC 48.5%, CRC 63.8%, and LC 87.1%). The slow-metabolizing ADH1B*1/*1 genotype was associated with high ORs for HNC (1.99; 95% CI 1.14-3.47) and EC (3.05; 1.87-4.99), but low ORs for GC (0.65; 0.45-0.95) and gastrectomy for peptic ulcer disease (0.59; 0.38-0.92). Gastrectomy, common among GC cases, accelerates alcohol delivery to the small intestine, increasing peak blood alcohol levels and exposure, and may offset the AD risk associated with ADH1B*1/*1. The inactive ALDH2*2 allele conferred elevated ORs for HNC (8.63; 4.90-15.21), EC (11.35; 6.78-18.99), GC (1.54; 1.08-2.19), and CRC (1.72; 1.01-2.91). The combined genotype (ADH1B*1/*1 and ALDH2*2) substantially increased ORs for HNC (17.05; 8.17-35.59) and EC (35.03; 17.38-70.65). Multiorgan cancerization was common along the digestive tract. The combined genotype increased ORs for multiorgan cancerization in HNC and EC, and ALDH2*2 increased ORs in GC and CRC.

conclusionGenotype strongly influences alcohol-related cancer risk, and many cancers occur during or after advanced alcohol use disorder.

Indexed as

Alcohol DehydrogenaseAlcoholismAldehyde Dehydrogenase, MitochondrialNeoplasmsAdultAgedEast Asian PeopleGenetic Predisposition to DiseaseGenotypeHumansJapanMaleMiddle AgedOdds RatioADH1B protein, humanAlcohol DehydrogenaseAldehyde Dehydrogenase, MitochondrialALDH2 protein, humanalcohol dehydrogenase‐1Balcohol dependencealdehyde dehydrogenase‐2cancer historyfield cancerization

Identifiers

PMID42415227
PMCPMC13341646

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