Tags

Type your tag names separated by a space and hit enter

Meat consumption, genetic susceptibility, and colon cancer risk: a United States multicenter case-control study.

Abstract

Meat consumption may especially increase risk of colon cancer when the meat is prepared at high temperatures and consumed by subjects with an inherited susceptibility to well-done meat. In this United States case-control study, the association between meat consumption, genetic susceptibility, and colon cancer risk was studied. Meat consumption data were available from a detailed diet history questionnaire and from questions about methods of preparation. Molecular variants in the carcinogen-metabolizing genes NAT2 and GSTM1 were determined in DNA extracted from WBCs. A total of 1542 cases and 1860 population-based controls were included in these analyses. The amount of red and white meat consumed was not associated with overall colon cancer risk. Processed meat consumption was weakly positively associated with colon cancer risk in men only (odds ratio for highest versus lowest quintile of intake = 1.4, 95% confidence interval = 1.0-1.9). The frequency of fried, broiled, baked, or barbecued meat, use of drippings, and doneness of meat were not significantly associated with risk. The Mutagen Index, as an estimate for exposure to mutagenic or carcinogenic substances, was slightly positively associated with colon cancer risk in men (odds ratio = 1.3, 95% confidence interval = 1.0-1.7). No significant associations with colon cancer risk were observed for different NAT2 and GSTM1 gene variants. The observed associations with processed meat and the Mutagen Index were strongest for those with the intermediate or rapid NAT2 acetylator phenotype. Associations were not markedly influenced by lack of the GSTM1 gene. This study provides little support for an association between meat consumption and colon cancer risk but does provide some, albeit not strong, evidence for a modifying effect of molecular variants of the NAT2 gene.

Links

  • FREE Publisher Full Text
  • Authors+Show Affiliations

    ,

    Fred Hutchinson Cancer Research Center, Cancer Prevention Research Program, Seattle, Washington 98109-1024, USA.

    , , , , ,

    Source

    MeSH

    Adult
    Aged
    Animals
    Arylamine N-Acetyltransferase
    Carcinogens
    Case-Control Studies
    Cattle
    Colonic Neoplasms
    Confidence Intervals
    Cooking
    DNA
    Environmental Exposure
    Feeding Behavior
    Female
    Fishes
    Genetic Predisposition to Disease
    Genetic Variation
    Glutathione Transferase
    Humans
    Male
    Meat
    Middle Aged
    Mutagens
    Odds Ratio
    Phenotype
    Poultry
    Risk Factors
    Sex Factors
    Surveys and Questionnaires
    United States

    Pub Type(s)

    Journal Article
    Multicenter Study
    Research Support, Non-U.S. Gov't
    Research Support, U.S. Gov't, P.H.S.

    Language

    eng

    PubMed ID

    9950235

    Citation

    Kampman, E, et al. "Meat Consumption, Genetic Susceptibility, and Colon Cancer Risk: a United States Multicenter Case-control Study." Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored By the American Society of Preventive Oncology, vol. 8, no. 1, 1999, pp. 15-24.
    Kampman E, Slattery ML, Bigler J, et al. Meat consumption, genetic susceptibility, and colon cancer risk: a United States multicenter case-control study. Cancer Epidemiol Biomarkers Prev. 1999;8(1):15-24.
    Kampman, E., Slattery, M. L., Bigler, J., Leppert, M., Samowitz, W., Caan, B. J., & Potter, J. D. (1999). Meat consumption, genetic susceptibility, and colon cancer risk: a United States multicenter case-control study. Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored By the American Society of Preventive Oncology, 8(1), pp. 15-24.
    Kampman E, et al. Meat Consumption, Genetic Susceptibility, and Colon Cancer Risk: a United States Multicenter Case-control Study. Cancer Epidemiol Biomarkers Prev. 1999;8(1):15-24. PubMed PMID: 9950235.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Meat consumption, genetic susceptibility, and colon cancer risk: a United States multicenter case-control study. AU - Kampman,E, AU - Slattery,M L, AU - Bigler,J, AU - Leppert,M, AU - Samowitz,W, AU - Caan,B J, AU - Potter,J D, PY - 1999/2/9/pubmed PY - 1999/2/9/medline PY - 1999/2/9/entrez SP - 15 EP - 24 JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology JO - Cancer Epidemiol. Biomarkers Prev. VL - 8 IS - 1 N2 - Meat consumption may especially increase risk of colon cancer when the meat is prepared at high temperatures and consumed by subjects with an inherited susceptibility to well-done meat. In this United States case-control study, the association between meat consumption, genetic susceptibility, and colon cancer risk was studied. Meat consumption data were available from a detailed diet history questionnaire and from questions about methods of preparation. Molecular variants in the carcinogen-metabolizing genes NAT2 and GSTM1 were determined in DNA extracted from WBCs. A total of 1542 cases and 1860 population-based controls were included in these analyses. The amount of red and white meat consumed was not associated with overall colon cancer risk. Processed meat consumption was weakly positively associated with colon cancer risk in men only (odds ratio for highest versus lowest quintile of intake = 1.4, 95% confidence interval = 1.0-1.9). The frequency of fried, broiled, baked, or barbecued meat, use of drippings, and doneness of meat were not significantly associated with risk. The Mutagen Index, as an estimate for exposure to mutagenic or carcinogenic substances, was slightly positively associated with colon cancer risk in men (odds ratio = 1.3, 95% confidence interval = 1.0-1.7). No significant associations with colon cancer risk were observed for different NAT2 and GSTM1 gene variants. The observed associations with processed meat and the Mutagen Index were strongest for those with the intermediate or rapid NAT2 acetylator phenotype. Associations were not markedly influenced by lack of the GSTM1 gene. This study provides little support for an association between meat consumption and colon cancer risk but does provide some, albeit not strong, evidence for a modifying effect of molecular variants of the NAT2 gene. SN - 1055-9965 UR - https://www.unboundmedicine.com/medline/citation/9950235/Meat_consumption_genetic_susceptibility_and_colon_cancer_risk:_a_United_States_multicenter_case_control_study_ L2 - http://cebp.aacrjournals.org/cgi/pmidlookup?view=long&pmid=9950235 DB - PRIME DP - Unbound Medicine ER -