Evidence map›Paper›PMID 17517051›Full record

ArticleCancer science2007

Alcohol dehydrogenase and aldehyde dehydrogenase polymorphisms and colorectal cancer: the Fukuoka Colorectal Cancer Study.

Guang Yin, Suminori Kono, Kengo Toyomura, Malcolm A Moore, June Nagano, Tetsuya Mizoue, Ryuichi Mibu, Masao Tanaka, Yoshihiro Kakeji, Yoshihiko Maehara and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 7 pooled it
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 7 syntheses or guidelines pooled it, 46 citations in OpenAlex.

  1. Association ofBioscience reports · 2019
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  3. Association between ALDHAfrican health sciences · 2017
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  8. Impact of Diarrhea after Drinking on Colorectal Tumor Risk: A Case Control StudyAsian Pacific journal of cancer prevention : APJCP · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 9 institutions in 5 countries.

Guang YinDepartment of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. yinguan@phealth.med.kyushu-u.ac.jp
Suminori Kono
Kengo Toyomura
Malcolm A Moore
June Nagano
Tetsuya Mizoue
Ryuichi Mibu
Masao Tanaka
Yoshihiro Kakeji
Yoshihiko Maehara
Takeshi Okamura
Koji Ikejiri
Kitaroh Futami
Yohichi Yasunami
Takafumi Maekawa
Kenji Takenaka
Hitoshi Ichimiya
Nobutoshi Imaizumi
General Department of Preventive Medicine · VNKyushu University · JPFukuoka University · JPFoundation for Ichthyosis and Related Skin Types · USFukuoka City Hospital · JPHamanomachi Hospital · JPKrankenhaus vom Roten Kreuz · DENational Hospital Organization Kyushu Cancer Center · JPNational Kyushu Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alcohol dehydrogenase and aldehyde dehydrogenase are key enzymes in alcohol metabolism and therefore may be of importance to colorectal cancer development. The present case-control study was conducted to determine the influence of ADH2, ADH3 and ALDH2 polymorphisms in Fukuoka, Japan, with 685 incident cases of histologically confirmed colorectal adenocarcinomas and 778 community controls selected randomly from the study area. Alcohol use was ascertained by in-person interview. Statistical adjustment was made for sex, age class, area, and alcohol use. Individuals with the allele 47Arg of the ADH2 polymorphism (slow metabolizers) had a statistically significant increase in risk, with an adjusted OR of 1.32 (95% CI = 1.07-1.63), compared with those having the ADH2*47His/His genotype. This association was not affected by the level of alcohol consumption. The ADH3 polymorphism showed no measurable association with the risk of colorectal cancer on either overall analysis or stratified analysis with alcohol use. The heterozygous ALDH2*487Glu/Lys genotype was not associated with an increase in the risk of colorectal cancer (adjusted OR 0.89, 95% CI = 0.71-1.13) compared with the ALDH2*487Glu/Glu genotype. Rather unexpectedly, the homozygous ALDH2*487Lys/Lys genotype was related to a statistically significantly decreased risk of colorectal cancer (adjusted OR 0.55, 95% CI = 0.33-0.93). It is unlikely that acetaldehyde metabolism determined by ALDH2 polymorphism contributes to the risk of colorectal cancer, whereas the role of ADH2 polymorphism deserves further investigation.

Indexed as

Polymorphism, GeneticAdenocarcinomaAdultAgedAlcohol DehydrogenaseAlcohol DrinkingAldehyde DehydrogenaseCase-Control StudiesColorectal NeoplasmsGenotypeHumansJapanMiddle AgedRiskADH1B protein, humanADH1C protein, humanAlcohol DehydrogenaseAldehyde Dehydrogenasecorneal protein 54, bovine

Identifiers

PMID17517051
PMCPMC11159727
OpenAlexW2073226547

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.