Rowena Chau1, Seyedeh Ghazaleh Dashti1, Driss Ait Ouakrim1, Daniel D Buchanan2, Mark Clendenning3, Christophe Rosty4, Ingrid M Winship5, Joanne P Young6, Graham G Giles7, Finlay A Macrae8, Alex Boussioutas9, Susan Parry10, Jane C Figueiredo11, A Joan Levine12, Dennis J Ahnen13, Graham Casey11, Robert W Haile12, Steven Gallinger14, Loïc Le Marchand15, Stephen N Thibodeau16, Noralane M Lindor17, Polly A Newcomb18, John D Potter19, John A Baron20, John L Hopper21, Mark A Jenkins1, Aung Ko Win22. 1. Centre for Molecular, Environmental, Genetic and Analytic Epidemiology. 2. Centre for Molecular, Environmental, Genetic and Analytic Epidemiology Colorectal Oncogenomics Group, Department of Pathology, University of Melbourne, Parkville, VIC, Australia. 3. Colorectal Oncogenomics Group, Department of Pathology, University of Melbourne, Parkville, VIC, Australia. 4. Colorectal Oncogenomics Group, Department of Pathology, University of Melbourne, Parkville, VIC, Australia School of Medicine, University of Queensland, Herston, QLD, Australia. 5. Department of Medicine Genetic Medicine and Family Cancer Clinic, Royal Melbourne Hospital, Parkville, VIC, Australia. 6. Departments of Haematology and Oncology, Queen Elizabeth Hospital SAHMRI Colorectal Node, Basil Hetzel Institute for Translational Research, Woodville, SA, Australia School of Medicine, University of Adelaide, Adelaide, SA, Australia. 7. Centre for Molecular, Environmental, Genetic and Analytic Epidemiology Cancer Epidemiology Centre, Cancer Council Victoria, Melbourne, VIC, Australia. 8. Department of Medicine Genetic Medicine and Family Cancer Clinic, Royal Melbourne Hospital, Parkville, VIC, Australia Colorectal Medicine and Genetics, Royal Melbourne Hospital, Parkville, VIC, Australia. 9. Department of Medicine Cancer Genomics and Predictive Medicine, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia. 10. New Zealand Familial Gastrointestinal Cancer Service, Auckland, New Zealand. 11. Norris Comprehensive Cancer Centre, University of Southern California, Los Angeles, CA, USA. 12. Department of Medicine, Stanford Cancer Institute, Stanford University, CA, USA. 13. Department of Medicine, University of Colorado School of Medicine, Denver, CO, USA. 14. Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, ON, Canada. 15. University of Hawaii Cancer Centre, Honolulu, Hawaii, USA. 16. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA. 17. Department of Health Science Research, Mayo Clinic Arizona, Scottsdale, AZ, USA. 18. Public Health Sciences Division, Fred Hutchinson Cancer Research Centre, Seattle, WA, USA School of Public Health, University of Washington, Seattle, WA, USA. 19. Public Health Sciences Division, Fred Hutchinson Cancer Research Centre, Seattle, WA, USA School of Public Health, University of Washington, Seattle, WA, USA Centre for Public Health Research, Massey University, Wellington, New Zealand. 20. Department of Medicine, University of North Carolina, Chapel Hill, Nc, USA. 21. Centre for Molecular, Environmental, Genetic and Analytic Epidemiology Department of Epidemiology and Institute of Health and Environment, School of Public Health, Seoul National University, Seoul, Korea. 22. Centre for Molecular, Environmental, Genetic and Analytic Epidemiology awin@unimelb.edu.au.
Abstract
BACKGROUND: People with a DNA mismatch repair (MMR) gene mutation have a substantially elevated risk of colorectal cancer (CRC) but the modifiers of this risk are not well established. We investigated the association between dietary supplement intake and CRC risk for carriers. METHODS: This study included 1966 (56% female) carriers of an MMR gene mutation (719 MLH1, 931 MSH2, 211 MSH6 and 105 PMS2) who were recruited from the USA, Canada, Australia and New Zealand into the Colon Cancer Family Registry between 1997 and 2012. Information on lifestyle factors including supplement intake was collected at the time of recruitment. Using Cox proportional hazards regression weighted to correct for ascertainment bias, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between self-reported multivitamin, calcium and folic acid supplement intake and CRC risk. RESULTS: Of 744 carriers with CRC, 18%, 6% and 5% reported intake of multivitamin, calcium and folic acid supplements for at least 1 month, respectively, compared with 27%, 11% and 10% of 1222 carriers without CRC. After adjusting for identified confounding variables, a decreased CRC risk was associated with multivitam inintake for at least 3 years (HR 0.47, 95% CI 0.32-0.69) and calcium intake for at least 3 years(HR 0.42, 95% CI 0.23-0.74), compared with never users. There was no evidence of an association between folic acid supplement intake and CRC risk (P = 0.82). CONCLUSION: Intake of multivitamin and calcium supplements might be associated with a decreased risk of CRC for MMR gene mutation carriers.
BACKGROUND:People with a DNA mismatch repair (MMR) gene mutation have a substantially elevated risk of colorectal cancer (CRC) but the modifiers of this risk are not well established. We investigated the association between dietary supplement intake and CRC risk for carriers. METHODS: This study included 1966 (56% female) carriers of an MMR gene mutation (719 MLH1, 931 MSH2, 211 MSH6 and 105 PMS2) who were recruited from the USA, Canada, Australia and New Zealand into the Colon Cancer Family Registry between 1997 and 2012. Information on lifestyle factors including supplement intake was collected at the time of recruitment. Using Cox proportional hazards regression weighted to correct for ascertainment bias, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between self-reported multivitamin, calcium and folic acid supplement intake and CRC risk. RESULTS: Of 744 carriers with CRC, 18%, 6% and 5% reported intake of multivitamin, calcium and folic acid supplements for at least 1 month, respectively, compared with 27%, 11% and 10% of 1222 carriers without CRC. After adjusting for identified confounding variables, a decreased CRC risk was associated with multivitam inintake for at least 3 years (HR 0.47, 95% CI 0.32-0.69) and calcium intake for at least 3 years(HR 0.42, 95% CI 0.23-0.74), compared with never users. There was no evidence of an association between folic acid supplement intake and CRC risk (P = 0.82). CONCLUSION: Intake of multivitamin and calcium supplements might be associated with a decreased risk of CRC for MMR gene mutation carriers.
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