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No evidence of gene-calcium interactions from genome-wide analysis of colorectal cancer risk.

About this Publication
Title
No evidence of gene-calcium interactions from genome-wide analysis of colorectal cancer risk.
Pubmed ID
25192705 (View this publication on the PubMed website)
Publication
Cancer Epidemiol. Biomarkers Prev. 2014 Dec; Volume 23 (Issue 12): Pages 2971-6
Authors
Du M, Zhang X, Hoffmeister M, Schoen RE, Baron JA, Berndt SI, Brenner H, Carlson CS, Casey G, Chan AT, Curtis KR, Duggan D, Gauderman WJ, Giovannucci EL, Gong J, Harrison TA, Hayes RB, Henderson BE, Hopper JL, Hsu L, ...show more Hudson TJ, Hutter CM, Jenkins MA, Jiao S, Kocarnik JM, Kolonel LN, Le Marchand L, Lin Y, Newcomb PA, Rudolph A, Seminara D, Thornquist MD, Ulrich CM, White E, Wu K, Zanke BW, Campbell PT, Slattery ML, Peters U, Chang-Claude J, Potter JD, Colon Cancer Family Registry and Genetics and Epidemiology of Colorectal Cancer Consortium
Affiliations
  • Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. School of Public Health, University of Washington, Seattle, Washington. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. mdu@fhcrc.org.
  • Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
  • Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Department of Medicine and Epidemiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
  • Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill, North Carolina.
  • Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
  • Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany. German Cancer Consortium (DKTK), Heidelberg, Germany.
  • Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington.
  • Department of Preventive Medicine, University of Southern California, Los Angeles, California.
  • Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
...show more
  • Genetic Basis of Human Disease, Translational Genomics Research Institute (TGen), Phoenix, Arizona.
  • Keck School of Medicine, University of Southern California, Los Angeles, California.
  • Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts.
  • Division of Epidemiology, Department of Population Health, New York University School of Medicine, New York, New York.
  • Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia.
  • Ontario Institute for Cancer Research, Toronto, Ontario, Canada. Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
  • Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland.
  • Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. School of Public Health, University of Washington, Seattle, Washington.
  • Epidemiology Program, University of Hawaii Cancer Center, Honolulu, Hawaii.
  • Division of Cancer Epidemiology, Unit of Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland.
  • Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. School of Public Health, University of Washington, Seattle, Washington. Division of Preventive Oncology, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT), Heidelberg, Germany.
  • Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts.
  • Division of Hematology, Faculty of Medicine, The University of Ottawa, Ottawa, Ontario, Canada.
  • Epidemiology Research Program, American Cancer Society, Atlanta, Georgia.
  • Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah.
  • Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. School of Public Health, University of Washington, Seattle, Washington. Centre for Public Health Research, Massey University, Wellington, New Zealand.
Abstract

BACKGROUND: Calcium intake may reduce risk of colorectal cancer, but the mechanisms remain unclear. Studies of interaction between calcium intake and SNPs in calcium-related pathways have yielded inconsistent results.

METHODS: To identify gene-calcium interactions, we tested interactions between approximately 2.7 million SNPs across the genome with self-reported calcium intake (from dietary or supplemental sources) in 9,006 colorectal cancer cases and 9,503 controls of European ancestry. To test for multiplicative interactions, we used multivariable logistic regression and defined statistical significance using the conventional genome-wide α = 5E-08.

RESULTS: After accounting for multiple comparisons, there were no statistically significant SNP interactions with total, dietary, or supplemental calcium intake.

CONCLUSIONS: We found no evidence of SNP interactions with calcium intake for colorectal cancer risk in a large population of 18,509 individuals.

IMPACT: These results suggest that in genome-wide analysis common genetic variants do not strongly modify the association between calcium intake and colorectal cancer in European populations.

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