Evidence map›Paper›PMID 17295732›Full record

ArticleAlcoholism, clinical and experimental research2007

Alcohol dehydrogenase genetic polymorphisms, low-to-moderate alcohol consumption, and risk of breast cancer.

Kala Visvanathan, Rosa M Crum, Paul T Strickland, Xiaojun You, Ingo Ruczinski, Sonja I Berndt, Anthony J Alberg, Sandra C Hoffman, George W Comstock, Douglas A Bell and 1 more

Abstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Kala VisvanathanDepartment of Epidemiology, The Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland 21205, USA. kvisvana@jhsph.edu
Rosa M Crum
Paul T Strickland
Xiaojun You
Ingo Ruczinski
Sonja I Berndt
Anthony J Alberg
Sandra C Hoffman
George W Comstock
Douglas A Bell
Kathy J Helzlsouer
Johns Hopkins University · USNational Institute of Environmental Health Sciences · US

Funding

INHERITED CANCER SUSCEPTIBILITY AND RELATION TO GENETIC DAMAGEZ01ES046008 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BELL, DOUGLAS · 1991 to 2008
$682k
ENVIRONMENTAL RISK FACTORS AND BREAST CANCER IN MARYLANDR01CA062988 · NCI · JOHNS HOPKINS UNIVERSITY · PI HELZLSOUER, KATHY J · 1993 to 1993
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ENVIRONMENTAL FACTORS AND BREAST CANCER RISK IN MARYLANDU01CA062988 · NCI · JOHNS HOPKINS UNIVERSITY · PI HELZLSOUER, KATHY J · 1993 to 1998
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Intramural NIH HHS Z01 ES046008NCI NIH HHS 5U0A1CA/ES62988NCI NIH HHS CA111948NCI NIH HHS P50 CA88843NIEHS NIH HHS ES060520
6 · The paper itself

Abstract

backgroundIn vitro, human isoenzymes encoded by genes homozygous for the ADH1C*1 or ADH1B*2 alleles metabolize ethanol to acetaldehyde at a faster rate than those homozygous for the ADH1C*2 or ADH1B*1 allele. Because alcohol is a known risk factor for breast cancer, we evaluated the joint association of genetic variants in ADH and alcohol consumption in relation to breast cancer.

methodsA nested case-control study of 321 cases and matched controls was conducted. Five single nucleotide polymorphisms (SNPs) in the ADH1C and ADH1B genes were genotyped. Logistic regression was used to assess odds ratios (ORs) and 95% confidence limits (CIs) for each SNP. Haplotype analysis of all 5 SNPs was also undertaken.

resultsAmong drinkers, the median intake of total alcohol was 13 g/wk (10th-90th percentiles; 4.5-135.9) in cases and 18 g/wk (10th-90th percentiles; 4.5-104.1) in controls. Women who drank alcohol tended to be at an increased risk of developing breast cancer compared with those who did not drink (OR=1.40%, 95% CI 0.97-2.03), particularly those who were premenopausal at the time of breast cancer diagnosis (OR=2.69%, 95% CI: 1.00-7.26). Of the known functional alleles, breast cancer risk was not significantly increased among carriers of at least 1 ADH1C*1 or ADH1B*2 allele, when compared with those homozygous for the genotype at each locus. However, breast cancer risk tended to be lower among women who inherited the G allele at ADH1B IVS1+896A>G (OR=0.62, 95% CI 0.37-1.04). Overall haplotype frequencies were not significantly different between cases and controls.

conclusionsIn this study low levels of alcohol are associated with a modest increase in breast cancer risk that is not altered by known functional allelic variants of the ADH1B and 1C gene. The protective association conferred by the G allele at ADH1B IVS1+896A>G needs further evaluation.

Indexed as

AgedAlcohol DehydrogenaseAlcohol DrinkingBreast NeoplasmsCase-Control StudiesFemaleGenotypeHumansMiddle AgedPolymorphism, Single NucleotideRisk FactorsAlcohol Dehydrogenase

Identifiers

PMID17295732
PMCPMC2787101
OpenAlexW2157345515

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.