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Cancer Epidemiol Biomarkers Prev. 2014 Sep;23(9):1824-33. doi: 10.1158/1055-9965.EPI-14-0062. Epub 2014 Jul 3.

Gene-environment interaction involving recently identified colorectal cancer susceptibility Loci.

Author information

1
Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington. ekantor@hsph.harvard.edu.
2
Division of Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland.
3
Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Public Health and Preventive Medicine, Oregon Health and Science University, Portland, Oregon.
4
Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland.
5
Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany. German Cancer Consortium (DKTK), Heidelberg, Germany.
6
Division of Research, Kaiser Permanente Medical Care Program, Oakland, California.
7
Epidemiology Research Program, American Cancer Society, Atlanta, Georgia.
8
Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington.
9
Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California.
10
Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
11
Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
12
Prevention and Cancer Control, Cancer Care Ontario, Toronto, Ontario, Canada.
13
Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
14
Translational Genomics Research Institute, Phoenix, Arizona.
15
Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts.
16
Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts.
17
Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington.
18
Division of Epidemiology, Department of Population Health, New York University School of Medicine, New York, New York.
19
Keck School of Medicine, University of Southern California, Los Angeles, California.
20
Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
21
Melbourne School of Population Health, The University of Melbourne, VIC, Australia.
22
Epidemiology Program, University of Hawaii Cancer Center, Honolulu, Hawaii.
23
Ontario Institute for Cancer Research, Toronto, Ontario, Canada.
24
Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
25
Department of Social and Preventive Medicine, University at Buffalo, Buffalo, New York.
26
Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington. Centre for Public Health Research, Massey University, Wellington, New Zealand.
27
Division of Cancer Epidemiology, Unit of Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany.
28
Department of Medicine and Epidemiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
29
Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah.
30
Department of Preventive Medicine, University of Tennessee Health Science Center, University of Tennessee, Memphis, Tennessee.
31
Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington. Division of Preventive Oncology, National Center for Tumor Diseases and German Cancer Research Center, Heidelberg, Germany.
32
Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada.
33
Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Department of Biostatistics, University of Washington School of Public Health, Seattle, Washington.

Abstract

BACKGROUND:

Genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) that are associated with risk of colorectal cancer. Prior research has evaluated the presence of gene-environment interaction involving the first 10 identified susceptibility loci, but little work has been conducted on interaction involving SNPs at recently identified susceptibility loci, including: rs10911251, rs6691170, rs6687758, rs11903757, rs10936599, rs647161, rs1321311, rs719725, rs1665650, rs3824999, rs7136702, rs11169552, rs59336, rs3217810, rs4925386, and rs2423279.

METHODS:

Data on 9,160 cases and 9,280 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) and Colon Cancer Family Registry (CCFR) were used to evaluate the presence of interaction involving the above-listed SNPs and sex, body mass index (BMI), alcohol consumption, smoking, aspirin use, postmenopausal hormone (PMH) use, as well as intake of dietary calcium, dietary fiber, dietary folate, red meat, processed meat, fruit, and vegetables. Interaction was evaluated using a fixed effects meta-analysis of an efficient Empirical Bayes estimator, and permutation was used to account for multiple comparisons.

RESULTS:

None of the permutation-adjusted P values reached statistical significance.

CONCLUSIONS:

The associations between recently identified genetic susceptibility loci and colorectal cancer are not strongly modified by sex, BMI, alcohol, smoking, aspirin, PMH use, and various dietary factors.

IMPACT:

Results suggest no evidence of strong gene-environment interactions involving the recently identified 16 susceptibility loci for colorectal cancer taken one at a time.

PMID:
24994789
PMCID:
PMC4209726
DOI:
10.1158/1055-9965.EPI-14-0062
[Indexed for MEDLINE]
Free PMC Article

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