ArticleCancer research2012
Characterization of gene-environment interactions for colorectal cancer susceptibility loci.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 17 of them syntheses that pooled 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.
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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.
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Who cites it
128 citing papers in PubMed, 17 syntheses or guidelines pooled it, 170 citations in OpenAlex.
- Meta-analysis of 16 studies of the association of alcohol with colorectal cancer.International journal of cancer · 2020Pooled it
- Gene-environment interactions and colorectal cancer risk: An umbrella review of systematic reviews and meta-analyses of observational studies.International journal of cancer · 2019Pooled it
- Influence of Smoking, Body Mass Index, and Other Factors on the Preventive Effect of Nonsteroidal Anti-Inflammatory Drugs on Colorectal Cancer Risk.Cancer research · 2018Pooled it
- Pooled it
- CYP24A1 variant modifies the association between use of oestrogen plus progestogen therapy and colorectal cancer risk.British journal of cancer · 2016Pooled it
- Effect of Proliferator-Activated Receptor-γ Pro12Ala Polymorphism on Colorectal Cancer Risk: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015Pooled it
- Analyzing large-scale samples confirms the association between rs16892766 polymorphism and colorectal cancer susceptibility.Scientific reports · 2015Pooled it
- Pooled it
- Pooled it
- Common variation rs6983267 at 8q24.1 and risk of colorectal adenoma and cancer: evidence based on 31 studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Association between IL-4 -589C>T polymorphism and colorectal cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Pooled it
- The association of matrix metalloproteinase-1 genetic polymorphism (-1607 1G>2G) with colorectal cancer: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Pooled it
- Cyclooxygenase-2 polymorphisms and susceptibility to colorectal cancer: a meta-analysis.Yonsei medical journal · 2013Pooled it
- Systematic review: diet-gene interactions and the risk of colorectal cancer.Alimentary pharmacology & therapeutics · 2013Pooled it
- Pooled it
- Replication study in Chinese population and meta-analysis supports association of the 11q23 locus with colorectal cancer.PloS one · 2012Pooled it
- Shaping the future of early-onset colorectal cancer prevention.Nature reviews. Cancer · 2026Review
- MyGeneRisk Colon: A Web-Based Tool for Personalized Colorectal Cancer Risk Prediction Based on Genetics and Lifestyle.medRxiv : the preprint server for health sciences · 2026Article
- Genetic risk factors modulate the association between physical activity and colorectal cancer.BMC medicine · 2026Article
68 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
46 authors at 6 institutions in 3 countries.
Funding
Abstract
Genome-wide association studies (GWAS) have identified more than a dozen loci associated with colorectal cancer (CRC) risk. Here, we examined potential effect-modification between single-nucleotide polymorphisms (SNP) at 10 of these loci and probable or established environmental risk factors for CRC in 7,016 CRC cases and 9,723 controls from nine cohort and case-control studies. We used meta-analysis of an efficient empirical-Bayes estimator to detect potential multiplicative interactions between each of the SNPs [rs16892766 at 8q23.3 (EIF3H/UTP23), rs6983267 at 8q24 (MYC), rs10795668 at 10p14 (FLJ3802842), rs3802842 at 11q23 (LOC120376), rs4444235 at 14q22.2 (BMP4), rs4779584 at 15q13 (GREM1), rs9929218 at 16q22.1 (CDH1), rs4939827 at 18q21 (SMAD7), rs10411210 at 19q13.1 (RHPN2), and rs961253 at 20p12.3 (BMP2)] and select major CRC risk factors (sex, body mass index, height, smoking status, aspirin/nonsteroidal anti-inflammatory drug use, alcohol use, and dietary intake of calcium, folate, red meat, processed meat, vegetables, fruit, and fiber). The strongest statistical evidence for a gene-environment interaction across studies was for vegetable consumption and rs16892766, located on chromosome 8q23.3, near the EIF3H and UTP23 genes (nominal P(interaction) = 1.3 × 10(-4); adjusted P = 0.02). The magnitude of the main effect of the SNP increased with increasing levels of vegetable consumption. No other interactions were statistically significant after adjusting for multiple comparisons. Overall, the association of most CRC susceptibility loci identified in initial GWAS seems to be invariant to the other risk factors considered; however, our results suggest potential modification of the rs16892766 effect by vegetable consumption.
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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.