Interaction between Red Meat Intake and NAT2 Genotype in Increasing the Risk of Colorectal Cancer in Japanese and African Americans
Wang H, Iwasaki M, Haiman CA, Kono S, Wilkens LR, Keku TO, Berndt SI, Tsugane S, Le Marchand L
PloS one · 18 citations
How it was studied
- Design
- Meta-analysis (indexed by PubMed)
- Studied in
- People
- Main outcome
- Clinical events such as disease or death
- Intake measured by
- Not stated
Who paid for it
- Funding
- Independent funding
- Government
- U.S. Department of Defense
- Government
- National Institutes of Health
- Government
- National Human Genome Research Institute
- Government
- National Cancer Institute
- Government
- National Institute of Diabetes and Digestive and Kidney Diseases
- Government
- NCI NIH HHS
- Government
- NHGRI NIH HHS
- Government
- NIDDK NIH HHS
- Grants
- National Cancer Institute (CA148085); National Cancer Institute (RC2CA148085); National Cancer Institute (R01 CA126895); National Cancer Institute (CA63464); U.S. Department of Defense (W81XWH0810383); National Cancer Institute (R01CA063464); National Cancer Institute (P30 CA016086); National Cancer Institute (R01-CA66635); National Cancer Institute (R37 CA054281); National Human Genome Research Institute (U01HG004726); National Cancer Institute (P30CA071789); National Human Genome Research Institute (HG004726); National Institute of Diabetes and Digestive and Kidney Diseases (P30‐DK‐034987); U.S. Department of Defense (W81XWH); National Cancer Institute (U01 CA164973); National Institutes of Health (CA1326792); National Cancer Institute (R01 CA066635); U.S. Department of Defense (CA54281); National Cancer Institute (CA 54281); National Institutes of Health (W81XWH); U.S. Department of Defense (CA63464); National Institutes of Health (P30 DK); National Cancer Institute (CA1326792); National Cancer Institute (U01 CA063464); National Cancer Institute (CA126895-S01); National Cancer Institute (R01 CA054281); National Institutes of Health (DK034987); National Institutes of Health (U01CA164973); National Institutes of Health (P30DK034987); National Institutes of Health (CA164973); National Institutes of Health (CA148085); National Institutes of Health (R01 CA 66635); National Institutes of Health (CA54281); National Institutes of Health (HG004726); National Institutes of Health (CA63464); National Institutes of Health (CA126895); National Institutes of Health (R01 CA126895)
Based on 8 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2015-12-18 · PLoS One · vol. 10 · issue 12 · p. e0144955
- Publisher
- Public Library of Science
- Cited
- 28 citations · more than 87% of similar papers · 1.8× the field average
- References
- 40 works
- Access
- Open access (journal) · PUBLIC-DOMAIN
- Research areas
- Nutrition, Genetics, and Disease · Biochemical Analysis and Sensing Techniques · Nutritional Studies and Diet
- Keywords
- Red meat, Colorectal cancer, Quartile, Genotype, Phenotype, Genotype-phenotype distinction, Medicine, Genotyping, Internal medicine, Biology, Cancer, Genetics, Food science, Gene, Confidence interval
- MeSH
- humans, colorectal neoplasms, genetic predisposition to disease, arylamine n-acetyltransferase, risk factors, genotype, polymorphism, single nucleotide, aged, middle aged, united states, japan, female, male, genome-wide association study, red meat, asian people, black or african american
9 authors
From US, JP
- Hansong WangUniversity of Hawaiʻi at Mānoa; University of Hawaii System; Cancer Center of Hawaii; University of Hawaii Cancer Center
- Motoki Iwasaki
- Christopher A. HaimanUniversity of Southern California
- Suminori KonoKyushu University
- Lynne Ross WilkensUniversity of Hawaiʻi at Mānoa; University of Hawaii System; Cancer Center of Hawaii; University of Hawaii Cancer Center
- Temitope O. KekuUniversity of North Carolina at Chapel Hill
Abstract
Heterocyclic aromatic amines formed in cooked meat may be an underlying mechanism for the red meat-colorectal cancer (CRC) association. These compounds require bioactivaction by N-acetyltransferase 2 (NAT2). An interaction effect between red meat consumption and NAT2 in increasing CRC risk has been inconsistently reported in whites. We investigated this interaction in two populations in which the high-activity rapid NAT2 phenotype is 10- and 2-fold more common than in whites. We meta-analyzed four studies of Japanese (2,217 cases, 3,788 controls) and three studies of African Americans (527 cases, 4,527 controls). NAT2 phenotype was inferred from an optimized seven-SNP genotyping panel. Processed and total red meat intakes were associated with an increased CRC risk in Japanese and in both ethnic groups combined (P's ≤ 0.002). We observed an interaction between processed meat intake and NAT2 in Japanese (P = 0.04), African Americans (P = 0.02), and in both groups combined (P = 0.006). The association of processed meat with CRC was strongest among individuals with the rapid NAT2 phenotype (combined analysis, OR for highest vs. lowest quartile: 1.62, 95% CI: 1.28-2.05; Ptrend = 8.0×10-5), intermediate among those with the intermediate NAT2 phenotype (1.29, 95% CI: 1.05-1.59; Ptrend = 0.05) and null among those with the slow phenotype (Ptrend = 0.45). A similar interaction was found for NAT2 and total red meat (Pinteraction = 0.03). Our findings support a role for NAT2 in modifying the association between red meat consumption and CRC in Japanese and African Americans.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC0).
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