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结直肠癌的炎症发病机制。

The inflammatory pathogenesis of colorectal cancer.

机构信息

Institute for Tumor Biology and Experimental Therapy, Georg-Speyer-Haus, Frankfurt/Main, Germany.

Frankfurt Cancer Institute, Goethe University Frankfurt, Frankfurt/Main, Germany.

出版信息

Nat Rev Immunol. 2021 Oct;21(10):653-667. doi: 10.1038/s41577-021-00534-x. Epub 2021 Apr 28.


DOI:10.1038/s41577-021-00534-x
PMID:33911231
Abstract

The mutational landscape of colorectal cancer (CRC) does not enable predictions to be made about the survival of patients or their response to therapy. Instead, studying the polarization and activation profiles of immune cells and stromal cells in the tumour microenvironment has been shown to be more informative, thus making CRC a prototypical example of the importance of an inflammatory microenvironment for tumorigenesis. Here, we review our current understanding of how colon cancer cells interact with their microenvironment, comprised of immune cells, stromal cells and the intestinal microbiome, to suppress or escape immune responses and how inflammatory processes shape the immune pathogenesis of CRC.

摘要

结直肠癌(CRC)的突变景观不能用来预测患者的生存或对治疗的反应。相反,研究肿瘤微环境中免疫细胞和基质细胞的极化和激活状态已被证明更具信息量,因此使 CRC 成为炎症微环境对肿瘤发生重要性的典型范例。在这里,我们回顾了我们目前对结肠癌细胞如何与其微环境相互作用的理解,该微环境由免疫细胞、基质细胞和肠道微生物组组成,以抑制或逃避免疫反应,以及炎症过程如何塑造 CRC 的免疫发病机制。

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本文引用的文献

[1]
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Nat Med. 2021-1

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Microbiota-derived metabolite promotes HDAC3 activity in the gut.

Nature. 2020-10

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