Department of Oncology, Johns Hopkins University, Baltimore, MD 21231, United States.
Department of Medicine, Howard University, Washington, DC 20060, United States.
World J Gastroenterol. 2022 Jul 7;28(25):2782-2801. doi: 10.3748/wjg.v28.i25.2782.
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.
在生命过程中,宿主炎症与肠道微生物群之间失调的相互作用增加了结直肠癌(CRC)的风险。虽然环境因素和非裔美国人(AA)的种族的社会经济现实仍然是 CRC 差异的主要原因,但本综述侧重于 CRC 差异的生物学介质,即对粘膜先天免疫的遗传祖先基因调控及其与微生物组的相互作用的认识不足。人们对免疫相关遗传多态性与微生物组多样性之间的联系机制的理解仍然很差,这些机制可能会影响慢性炎症并加剧 AA 中的 CRC 差异。更好地了解宿主遗传学、细菌和 CRC 发病机制之间的关系将提高对整个种族/族群的癌症风险的预测。