Evidence map›Paper›PMID 26072521›Full record

ArticleJournal of the National Cancer Institute2015

A Candidate-Pathway Approach to Identify Gene-Environment Interactions: Analyses of Colon Cancer Risk and Survival.

Noha Sharafeldin, Martha L Slattery, Qi Liu, Conrado Franco-Villalobos, Bette J Caan, John D Potter, Yutaka Yasui

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the National Cancer Institute, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–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

19 citing papers in PubMed.

  1. Article
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  6. Review
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  9. Observational
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  17. Diet, nutrition, and cancer: past, present and future.Nature reviews. Clinical oncology · 2016
    Review
  18. Article
  19. 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

7 authors.

Noha SharafeldinSchool of Public Health, University of Alberta, Edmonton, Alberta, Canada (NS, QL, CFV, YY); Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT (MLS); Division of Research, Kaiser Permanente Medical Care Program, Oakland, CA (BJC); Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA (JDP); Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA (JDP); Centre for Public Health Research, Massey University, Wellington, New Zealand (JDP).
Martha L SlatterySchool of Public Health, University of Alberta, Edmonton, Alberta, Canada (NS, QL, CFV, YY); Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT (MLS); Division of Research, Kaiser Permanente Medical Care Program, Oakland, CA (BJC); Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA (JDP); Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA (JDP); Centre for Public Health Research, Massey University, Wellington, New Zealand (JDP).
Qi LiuSchool of Public Health, University of Alberta, Edmonton, Alberta, Canada (NS, QL, CFV, YY); Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT (MLS); Division of Research, Kaiser Permanente Medical Care Program, Oakland, CA (BJC); Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA (JDP); Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA (JDP); Centre for Public Health Research, Massey University, Wellington, New Zealand (JDP).
Conrado Franco-VillalobosSchool of Public Health, University of Alberta, Edmonton, Alberta, Canada (NS, QL, CFV, YY); Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT (MLS); Division of Research, Kaiser Permanente Medical Care Program, Oakland, CA (BJC); Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA (JDP); Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA (JDP); Centre for Public Health Research, Massey University, Wellington, New Zealand (JDP).
Bette J CaanSchool of Public Health, University of Alberta, Edmonton, Alberta, Canada (NS, QL, CFV, YY); Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT (MLS); Division of Research, Kaiser Permanente Medical Care Program, Oakland, CA (BJC); Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA (JDP); Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA (JDP); Centre for Public Health Research, Massey University, Wellington, New Zealand (JDP).
John D PotterSchool of Public Health, University of Alberta, Edmonton, Alberta, Canada (NS, QL, CFV, YY); Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT (MLS); Division of Research, Kaiser Permanente Medical Care Program, Oakland, CA (BJC); Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA (JDP); Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA (JDP); Centre for Public Health Research, Massey University, Wellington, New Zealand (JDP).
Yutaka YasuiSchool of Public Health, University of Alberta, Edmonton, Alberta, Canada (NS, QL, CFV, YY); Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT (MLS); Division of Research, Kaiser Permanente Medical Care Program, Oakland, CA (BJC); Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA (JDP); Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA (JDP); Centre for Public Health Research, Massey University, Wellington, New Zealand (JDP). yyasui@ualberta.ca sharafeldin.n@ualberta.ca.

Funding

DIET, ACTIVITY &REPRODUCTION--RISKS FOR RECTAL CANCERR01CA048998 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA L · 1991 to 2012
$7.9M
SURVEILLANCE EPIDEMIOLOGY &END RESULTS PROGRAMN01PC067000 · PC · UNIVERSITY OF UTAH · PI WIGGINS, CHARLES L · 1996 to 2000
$1.3M
DIET, ACTIVITY &REPRODUCTION--RISKS FOR RECTAL CANCERU01CA048998 · NCI · UNIVERSITY OF UTAH · PI SLATTERY, MARTHA OR MARTY L · 1997 to 1999
–
Canadian Institutes of Health ResearchNCI NIH HHS CA48998NCI NIH HHS CA615757NCI NIH HHS N01-PC-67000
6 · The paper itself

Abstract

backgroundGenetic association studies have traditionally focused on associations between individual single nucleotide polymorphisms (SNPs) and disease. Standard analysis ignores interactions between multiple SNPs and environmental exposures explaining a small portion of disease heritability: the often-cited issue of "missing heritability."

methodsWe present a novel three-step analytic framework for modeling gene-environment interactions (GEIs) between an angiogenesis candidate-gene pathway and three lifestyle exposures (dietary protein, smoking, and alcohol consumption) on colon cancer risk and survival. Logic regression was used to summarize the gene-pathway effects, and GEIs were modeled using logistic regression and Cox proportional hazards models. We analyzed data from 1541 colon cancer case patients and 1934 control subjects in the Diet, Activity and Lifestyle as a Risk Factor for Colon Cancer Study.

resultsWe identified five statistically significant GEIs for colon cancer risk. For risk interaction, odds ratios (ORINT) and 95% confidence intervals (CIs) were FLT1(rs678714) and BMP4(rs17563) and smoking (ORINT = 1.64, 95% CI = 1.11 to 2.41 and ORINT = 1.60, 95% CI = 1.10 to 2.32, respectively); FLT1(rs2387632 OR rs9513070) and protein intake (ORINT = 1.69, 95% CI = 1.03 to 2.77); KDR(rs6838752) and TLR2(rs3804099) and alcohol (ORINT = 1.53, 95% CI = 1.10 to 2.13 and ORINT = 1.59, 95% CI = 1.05 to 2.38, respectively). Three GEIs between TNF, BMP1, and BMPR2 genes and the three exposures were statistically significant at the 5% level in relation to colon cancer survival but not after multiple-testing adjustment.

conclusionsAdopting a comprehensive biologically informed candidate-pathway approach identified GEI effects on colon cancer. Findings may have important implications for public health and personalized medicine targeting prevention and therapeutic strategies. Findings from this study need to be validated in other studies.

Indexed as

Gene-Environment InteractionPolymorphism, Single NucleotideAdultAgedAlcohol DrinkingBone Morphogenetic Protein 1Bone Morphogenetic Protein Receptors, Type IIColonic NeoplasmsDietary ProteinsFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGenotypeHumansLogistic ModelsMaleBMP1 protein, humanBMPR2 protein, humanBone Morphogenetic Protein 1Bone Morphogenetic Protein Receptors, Type IIDietary ProteinsTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID26072521
PMCPMC4651103

What OpenQuestion holds

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Registered trials

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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.