Published online Jul 7, 2022. doi: 10.3748/wjg.v28.i25.2782
Peer-review started: October 28, 2021
First decision: December 26, 2021
Revised: January 27, 2022
Accepted: May 26, 2022
Article in press: May 26, 2022
Published online: July 7, 2022
Processing time: 248 Days and 14.5 Hours
Dysregulated interactions between host inflammation and gut microbiota over the course of life increase the risk of colorectal cancer (CRC). While environmental factors and socio-economic realities of race remain predominant contributors to CRC disparities in African-Americans (AAs), this review focuses on the biological mediators of CRC disparity, namely the under-appreciated influence of inherited ancestral genetic regulation on mucosal innate immunity and its interaction with the microbiome. There remains a poor understanding of mechanisms linking immune-related genetic polymorphisms and microbiome diversity that could influence chronic inflammation and exacerbate CRC disparities in AAs. A better understanding of the relationship between host genetics, bacteria, and CRC pathogenesis will improve the prediction of cancer risk across race/ethnicity groups overall.
Core Tip: Studies largely examine either variations in microbiome composition or host immunity polymorphisms, often using genome-wide association studies comprised of populations mainly of European ancestry. There is, thus, a pressing need for studies that include, recruit, and account for more widely diverse cohorts. Identification of population-associated polymorphisms driving host/microbiome interactions linked to colorectal cancer (CRC) disparity may reveal genes or pathways that could be targeted for patient-specific CRC interception strategies.