Journal article
Alcohol consumption and the risk of colorectal cancer for mismatch repair gene mutation carriers
S Ghazaleh Dashti, DD Buchanan, H Jayasekara, DA Ouakrim, M Clendenning, C Rosty, IM Winship, FA MacRae, GG Giles, S Parry, G Casey, RW Haile, S Gallinger, L Le Marchand, SN Thibodeau, NM Lindor, PA Newcomb, JD Potter, JA Baron, JL Hopper Show all
Cancer Epidemiology Biomarkers and Prevention | AMER ASSOC CANCER RESEARCH | Published : 2017
Abstract
Background: People with germline mutation in one of the DNA mismatch repair (MMR) genes have increased colorectal cancer risk. For these high-risk people, study findings of the relationship between alcohol consumption and colorectal cancer risk have been inconclusive. Methods: 1,925 MMR gene mutations carriers recruited into the Colon Cancer Family Registry who had completed a questionnaire on lifestyle factors were included. Weighted Cox proportional hazard regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between alcohol consumption and colorectal cancer. Results: Colorectal cancer was diagnosed in 769 carriers (40%) at a mean ..
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Grants
Awarded by National Cancer Institute
Funding Acknowledgements
This work was supported by grant UM1CA167551 from the National Cancer Institute and through cooperative agreements with the following Colon Cancer Family Registry centers: Australasian Colorectal Cancer Family Registry (U01 CA074778 and U01/U24 CA097735); Mayo Clinic Cooperative Family Registry for Colon Cancer Studies (U01/U24 CA074800); Ontario Familial Colorectal Cancer Registry (U01/U24 CA074783); Seattle Colorectal Cancer Family Registry (U01/U24 CA074794); University of Hawaii Colorectal Cancer Family Registry (U01/U24 CA074806); and USC Consortium Colorectal Cancer Family Registry U01/U24 CA074799).r Seattle CCFR research was also supported by the Cancer Surveillance System of the Fred Hutchinson Cancer Research Center, which was funded by Control Nos. N01-CN-67009 (1996-2003) and N01-PC-35142 (2003-2010) and Contract No. HHSN2612013000121 (2010-2017) from the Surveillance, Epidemiology and End Results (SEER) Program of the National Cancer Institute with additional support from the Fred Hutchinson Cancer Research Center.r The collection of cancer incidence data used in this study was supported by the California Department of Public Health as part of the state-wide cancer reporting program mandated by California Health and Safety Code Section 103885; the National Cancer Institute's Surveillance, Epidemiology and End Results Program under contract HHSN261201000140C awarded to the Cancer Prevention Institute of California, contract HHSN261201000035C awarded to the University of Southern California, and contract HHSN261201000034C awarded to the Public Health Institute; and the Centers for Disease Control and Prevention's National Program of Cancer Registries, under agreement U58DP003862-01 awarded to the California Department of Public Health. The ideas and opinions expressed herein are those of the author(s) and endorsement by the State of California, Department of Public Health the National Cancer Institute, and the Centers for Disease Control and Prevention or their Contractors and Subcontractors is not intended nor should be inferred.r This study was also supported by Centre for Research Excellence grant APP1042021 and Program Grant APP1074383 from the National Health and Medical Research Council (NHMRC), Australia.