Lopez Anthony, Hansmannel Franck, Kokten Tunay, Bronowicki Jean-Pierre, Melhem Hassan, Sokol Harry, Peyrin-Biroulet Laurent
Department of Gastroenterology and Hepatology and Inserm U954, Nancy University Hospital, Lorraine University, France.
Department of Research Inserm U954, Lorraine University, France.
Carcinogenesis. 2017 Dec 7;38(12):1157-1166. doi: 10.1093/carcin/bgx087.
Evolution led to an essential symbiotic relationship between the host and commensal microbiota, regulating physiological functions including inflammation and immunity. This equilibrium can be disturbed by environmental factors such as lifestyle, diet or antibiotic pressure, contributing to create a dysbiosis. There is much evidence about the gut microbiota's contribution to carcinogenesis, involving pro-inflammatory and immunosuppressive signals. At the same time, it seems to be increasingly clear that commensal microbes can modulate cancer therapy efficacy and safety, in particular, innovating treatments as immune checkpoint inhibitors. In this review, we discuss how the microbiota can promote digestive tract carcinogenesis, responsiveness to cancer therapeutics and cancer-associated complications.
进化导致宿主与共生微生物群之间形成了一种重要的共生关系，调节包括炎症和免疫在内的生理功能。这种平衡可能会受到生活方式、饮食或抗生素压力等环境因素的干扰，从而导致生态失调。有大量证据表明肠道微生物群对致癌作用有影响，涉及促炎和免疫抑制信号。与此同时，越来越明显的是，共生微生物可以调节癌症治疗的疗效和安全性，特别是像免疫检查点抑制剂这样的创新疗法。在这篇综述中，我们讨论了微生物群如何促进消化道致癌、对癌症治疗的反应以及癌症相关并发症。
