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肠道微生物群与结直肠癌

Gut microbiota and colorectal cancer.

作者信息

Gao R, Gao Z, Huang L, Qin H

机构信息

Tongji University School of Medicine affiliated Tenth People's Hospital, No.301 Middle Yanchang Road, Shanghai, 200072, China.

出版信息

Eur J Clin Microbiol Infect Dis. 2017 May;36(5):757-769. doi: 10.1007/s10096-016-2881-8. Epub 2017 Jan 7.

Abstract

The gut microbiota is considered as a forgotten organ in human health and disease. It maintains gut homeostasis by various complex mechanisms. However, disruption of the gut microbiota has been confirmed to be related to gastrointestinal diseases such as colorectal cancer, as well as remote organs in many studies. Colorectal cancer is a multi-factorial and multi-stage involved disorder. The role for microorganisms that initiate and facilitate the process of colorectal cancer has become clear. The candidate pathogens have been identified by culture and next sequencing technology. Persuasive models have also been proposed to illustrate the complicated and dynamic time and spatial change in the carcinogenesis. Related key molecules have also been investigated to demonstrate the pathways crucial for the development of colorectal cancer. In addition, risk factors that contribute to the tumorigenesis can also be modulated to decrease the susceptibility for certain population. In addition, the results of basic studies have also translated to clinical application, which displayed a critical value for the diagnosis and therapy of colorectal cancer. In this review, we not only emphasize the exploration of the mechanisms, but also potential clinical practice implication in this microbiota era.

摘要

肠道微生物群被认为是人类健康与疾病中一个被遗忘的器官。它通过各种复杂机制维持肠道稳态。然而,在许多研究中,肠道微生物群的破坏已被证实与诸如结直肠癌等胃肠道疾病以及远端器官有关。结直肠癌是一种涉及多因素和多阶段的疾病。启动并促进结直肠癌进程的微生物的作用已变得清晰。通过培养和下一代测序技术已鉴定出候选病原体。还提出了有说服力的模型来说明致癌过程中复杂且动态的时间和空间变化。也对相关关键分子进行了研究,以证明对结直肠癌发展至关重要的途径。此外,还可以调节促成肿瘤发生的风险因素,以降低特定人群的易感性。此外,基础研究的结果也已转化为临床应用,这对结直肠癌的诊断和治疗显示出关键价值。在本综述中,我们不仅强调对机制的探索,还强调在这个微生物群时代潜在的临床实践意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee96/5395603/32496166f25c/10096_2016_2881_Fig1_HTML.jpg

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