Evidence map›Paper›PMID 23216531›Full record

SynthesisAlimentary pharmacology & therapeutics2013

Systematic review: diet-gene interactions and the risk of colorectal cancer.

V Andersen, R Holst, U Vogel

Open access · bronzeAbstract readSystematic Review
In one paragraph

Synthesis in Alimentary pharmacology & therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 7 pooled it
4.5field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 7 syntheses or guidelines pooled it, 47 citations in OpenAlex.

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  6. Meta-analysis of the association between NQO1 Pro187Ser polymorphism and colorectal cancer in Asians.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  7. Associations of CYP2E1 rs2031920 and rs3813867 polymorphisms with colorectal cancer risk: a systemic review and meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
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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

3 authors at 2 institutions in 1 country.

V AndersenMedical Department, Hospital of Southern Jutland, Aabenraa, Denmark. vandersen@health.sdu.dk
R Holst
U Vogel
University of Southern Denmark · DKNational Research Centre for the Working Environment · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiet contributes significantly to colorectal cancer (CRC) aetiology and may be potentially modifiable.

aimTo review diet-gene interactions, aiming to further the understanding of the underlying biological pathways in CRC development.

methodsThe PubMed and Medline were systematically searched for prospective studies in relation to diet, colorectal cancer and genetics.

resultsIn a meta-analysis, no interaction between NAT1 phenotypes and meat intake in relation to risk of CRC was found (P-value for interaction 0.95). We found a trend towards interaction between NAT2 phenotypes and meat intake in relation to risk of CRC. High meat intake was not associated with risk of CRC among carriers of the slow NAT2 phenotype, whereas NAT2 fast acetylators with high meat intake were at increased risk of CRC (OR = 1.25; 95% confidence interval (CI): 0.92-2.01) compared with slow acetylators with low meat intake (reference), P-value for interaction = 0.07. Low meat intake in the studied populations may influence the result. Interactions between meat, cruciferous vegetables, fibres, calcium, vitamins, and alcohol and ABCB1, NFKB1, GSTM1, GSTT1, CCND1, VDR, MGTM, IL10 and PPARG are suggested.

conclusionsA number of interactions between genetic variation and diet are suggested, but the findings need replication in independent, prospective, and well-characterised cohorts before conclusions regarding the underlying biological mechanisms can be reached. When the above criteria are met, studies on diet-gene interactions may contribute valuable insight into the biological mechanisms underlying the role of various dietary items in colorectal carcinogenesis.

Indexed as

DietGenetic VariationColorectal NeoplasmsFeeding BehaviorHumansRisk Factors

Identifiers

PMID23216531
PMCPMC3565452
OpenAlexW2066902086

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.