Journal
GASTROENTEROLOGY
Volume 163, Issue 4, Pages 862-874Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.gastro.2022.06.054
Keywords
Immunology; Microbiome; Molecular Pathological Epidemiology
Categories
Funding
- National Institutes of Health (NIH) [P01 CA87969, UM1 CA186107, P01 CA55075, UM1 CA167552, U01 CA167552, P50 CA127003, R01 CA118553, R01 CA169141, R01 CA137178, K24 DK098311, R35 CA197735, R01 CA151993, K07 CA188126]
- Cancer Research UK Grand Challenge Award (UK) [C10674/A27140]
- Stand Up to Cancer (SU2C) Colorectal Cancer Dream Team Translational Research Grant [SU2C-AACR-DT22-17]
- Project P Fund
- Friends of the Dana-Farber Cancer Institute
- Bennett Family Fund
- Entertainment Industry Foundation through the National Colorectal Cancer Research Alliance
- Overseas Research Fellowship from Japan Society for the Promotion of Science [201860083, 201960541]
- Huazhong University of Science and Technology
- Uehara Memorial Foundation
- Yasuda Medical Foundation
- Mitsukoshi Health and Welfare Foundation
- Douglas Gray Woodruff Chair fund
- Guo Shu Shi Fund
- Anonymous Family Fund for Innovations in Colorectal Cancer
- George Stone Family Foundation
- Conquer Cancer Foundation of American Society of Clinical Oncology Career Development Award
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This study found that a Western-style diet is associated with a higher incidence of colorectal cancer containing abundant pks(+) E coli, providing further support for a potential link between diet, the intestinal microbiota, and colorectal carcinogenesis.
BACKGROUND & AIMS: Evidence supports a carcinogenic role of Escherichia coli carrying the pks island that encodes enzymes for colibactin biosynthesis. We hypothesized that the association of the Western-style diet (rich in red and processed meat) with colorectal cancer incidence might be stronger for tumors containing higher amounts of pks(+) E coli. METHODS: Western diet score was calculated using food frequency questionnaire data obtained every 4 years during follow-up of 134,775 participants in 2 United States-wide prospective cohort studies. Using quantitative polymerase chain reaction, we measured pks(+) E coli DNA in 1175 tumors among 3200 incident colorectal cancer cases that had occurred during the follow-up. We used the 3200 cases and inverse probability weighting (to adjust for selection bias due to tissue availability), integrated in multivariable-adjusted duplication-method Cox proportional hazards regression analyses. RESULTS: The association of the Western diet score with colorectal cancer incidence was stronger for tumors containing higher levels of pks(+) E coli (P-heterogeneity = .014). Multivariable-adjusted hazard ratios (with 95% confidence interval) for the highest (vs lowest) tertile of the Western diet score were 3.45 (1.53-7.78) (P-trend = 0.001) for pks(+) E coli-high tumors, 1.22 (0.57-2.63) for pks(+) E coil-low tumors, and 1.10 (0.85-1.42) for pks(+) E coli-negative tumors. The pks(+) E coli level was associated with lower disease stage but not with tumor location, microsatellite instability, or BRAF, KRAS, or PIK3CA mutations. CONCLUSIONS: The Western-style diet is associated with a higher incidence of colorectal cancer containing abundant pks(+) E coli, supporting a potential link between diet, the intestinal microbiota, and colorectal carcinogenesis.
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