Evidence map›Paper›PMID 19068087›Full record

ArticleCancer science2009

Impact of alcohol consumption with polymorphisms in alcohol-metabolizing enzymes on pancreatic cancer risk in Japanese.

Junya Kanda, Keitaro Matsuo, Takeshi Suzuki, Takakazu Kawase, Akio Hiraki, Miki Watanabe, Nobumasa Mizuno, Akira Sawaki, Kenji Yamao, Kazuo Tajima and 1 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 4 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

29 citing papers in PubMed, 4 syntheses or guidelines pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Association ofBioscience reports · 2019
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Review
  7. Alcohol Consumption and Autoimmune Diseases.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Environmental Risk Factors of Pancreatic Cancer.Journal of clinical medicine · 2019
    Review
  20. Article
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

11 authors at 2 institutions in 1 country.

Junya KandaDivision of Epidemiology and Prevention, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya, Japan.
Keitaro Matsuo
Takeshi Suzuki
Takakazu Kawase
Akio Hiraki
Miki Watanabe
Nobumasa Mizuno
Akira Sawaki
Kenji Yamao
Kazuo Tajima
Hideo Tanaka
Aichi Cancer Center · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The putative impact of alcohol on pancreatic cancer (PC) risk remains controversial. Here, we conducted a case-control study in Japanese to assess the impact of alcohol in conjunction with polymorphisms in alcohol-metabolizing enzymes. Cases were 160 patients with pancreatic cancer at Aichi Cancer Center, Nagoya, Japan. Two control groups of 800 age- and sex-matched non-cancer subjects each were independently selected. The impact of alcohol and polymorphisms in aldehyde dehydrogenase 2 (ALDH2) Glu504Lys, alcohol dehydrogenase (ADH) 1B His48Arg, and ADH1C Arg272Gln on PC risk was examined with multivariate analysis adjusted for potential confounders to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results showed no independent impact of alcohol or genotype on PC risk except former drinking. To avoid reverse causation, former drinkers were excluded in further analyses. In the analysis of the combined effects of alcohol consumption and genotype, significant impact of alcohol was seen for those subjects with ALDH2 Lys+ allele, ADH1B His/His, or ADH1C Arg/Arg (trend P = 0.077, 0.003, or 0.020, respectively), each of which is associated with a high concentration or rapid production of acetaldehyde. Analysis of genotype combinations showed that ‘ever drinking’ with both ADH1B His/His and ALDH2 Lys + was the most potent risk factor for PC relative to ‘never drinkers’ with both ADH1B His/His and ALDH2 Glu/Glu [OR (95% CI); 4.09 (1.30–12.85)]. These results indicate that alcohol has an impact on PC risk when the effects of alcohol consumption and metabolism are combined. Acetaldehyde may be involved in the mechanisms underlying PC development.

Indexed as

AcetaldehydeAdultAgedAlcohol DehydrogenaseAlcohol DrinkingAldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialAsian PeopleCase-Control StudiesCohort StudiesDNA, NeoplasmFemaleFollow-Up StudiesGenotypeHumansJapanAcetaldehydeADH1B protein, humanADH1C protein, humanAlcohol DehydrogenaseAldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialALDH2 protein, humanDNA, Neoplasm

Identifiers

PMID19068087
PMCPMC11159673
OpenAlexW1969275265

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.