Evidence map›Paper›PMID 19434079›Full record

ReviewNature reviews. Genetics2009

New insights into the aetiology of colorectal cancer from genome-wide association studies.

Albert Tenesa, Malcolm G Dunlop

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
199citing papers in PubMed, 10 pooled it
–field-weighted citation impact
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

199 citing papers in PubMed, 10 syntheses or guidelines pooled it.

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  10. Characterization of 9p24 risk locus and colorectal adenoma and cancer: gene-environment interaction and meta-analysis.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2010
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  15. Cyclooxygenase-2 polymorphisms, aspirin treatment, and risk for colorectal adenoma recurrence--data from a randomized clinical trial.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2009
    Trial
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139 more citing papers are in PubMed but not listed here.

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

2 authors.

Albert TenesaColon Cancer Genetics Group, University of Edinburgh, Western General Hospital, Edinburgh, UK. Albert.Tenesa@ed.ac.uk
Malcolm G Dunlop

Funding

Cancer Research UK C348/A8896Cancer Research UK C48/A6361Chief Scientist Office CZB/4/449Medical Research Council MC_U127527198
6 · The paper itself

Abstract

Genome-wide association studies have recently identified ten common genetic variants associated with colorectal cancer susceptibility, several suggesting the involvement of components of the transforming growth factor beta (TGFbeta) superfamily signalling pathway. To date, no causal sequence variants have been identified, and risk seems to be mediated through effects on gene regulation. Several markers are located close to poorly characterized genes or in gene deserts, raising challenges for elucidating mechanisms of susceptibility. Disease-associated common genetic variation offers the potential to refine risk stratification within populations and enable more targeted disease prevention strategies.

Indexed as

Genome-Wide Association StudyColorectal NeoplasmsGenetic Predisposition to DiseaseHumansRisk Factors

Identifiers

PMID19434079

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.