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微生物群作为癌症进展和治疗的介质。

Microbiota as a mediator of cancer progression and therapy.

作者信息

Pope Jillian L, Tomkovich Sarah, Yang Ye, Jobin Christian

机构信息

Department of Medicine, University of Florida, Gainesville, Fla.

Department of Medicine, University of Florida, Gainesville, Fla; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC.

出版信息

Transl Res. 2017 Jan;179:139-154. doi: 10.1016/j.trsl.2016.07.021. Epub 2016 Aug 3.

DOI:10.1016/j.trsl.2016.07.021
PMID:27554797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5674984/
Abstract

Complex and intricate circuitries regulate cellular proliferation, survival, and growth, and alterations of this network through genetic and epigenetic events result in aberrant cellular behaviors, often leading to carcinogenesis. Although specific germline mutations have been recognized as cancer inducers, the vast majority of neoplastic changes in humans occur through environmental exposure, lifestyle, and diet. An emerging concept in cancer biology implicates the microbiota as a powerful environmental factor modulating the carcinogenic process. For example, the intestinal microbiota influences cancer development or therapeutic responses through specific activities (immune responses, metabolites, microbial structures, and toxins). The numerous effects of microbiota on carcinogenesis, ranging from promoting, preventing, or even influencing therapeutic outcomes, highlight the complex relationship between the biota and the host. In this review, we discuss the latest findings on this complex microbial interaction with the host and highlight potential mechanisms by which the microbiota mediates such a wide impact on carcinogenesis.

摘要

复杂而精细的信号通路调控着细胞的增殖、存活和生长,通过遗传和表观遗传事件导致该网络的改变会引发异常的细胞行为,常常导致癌症的发生。尽管特定的种系突变已被确认为癌症诱导因素,但人类绝大多数肿瘤性变化是通过环境暴露、生活方式和饮食发生的。癌症生物学中一个新兴的概念认为,微生物群是调节致癌过程的一个强大环境因素。例如,肠道微生物群通过特定活动(免疫反应、代谢产物、微生物结构和毒素)影响癌症的发展或治疗反应。微生物群对致癌作用的众多影响,从促进、预防甚至影响治疗结果,突出了生物群与宿主之间的复杂关系。在这篇综述中,我们讨论了关于这种与宿主复杂的微生物相互作用的最新发现,并强调了微生物群介导对致癌作用产生如此广泛影响的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/83251415dcf5/nihms807821f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/b2328fc66e0d/nihms807821f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/3fb8fd467f6a/nihms807821f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/c10a4276912c/nihms807821f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/83251415dcf5/nihms807821f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/b2328fc66e0d/nihms807821f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/3fb8fd467f6a/nihms807821f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/c10a4276912c/nihms807821f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5c5/5674984/83251415dcf5/nihms807821f4.jpg

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