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癌症中的应激与耐药性

Stress and drug resistance in cancer.

作者信息

Flaherty Renée L, Falcinelli Marta, Flint Melanie S

机构信息

School of Pharmacy and Biomolecular Sciences, University of Brighton, Moulsecoomb, Brighton, BN2 4GJ, UK.

出版信息

Cancer Drug Resist. 2019 Sep 19;2(3):773-786. doi: 10.20517/cdr.2019.016. eCollection 2019.

DOI:10.20517/cdr.2019.016
PMID:35582576
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8992509/
Abstract

Patients diagnosed with cancer often undergo considerable psychological distress, and the induction of the psychological stress response has been linked with a poor response to chemotherapy. The psychological stress response is mediated by fluctuations of the hormones glucocorticoids (GCs) and catecholamines. Binding to their respective receptors, GCs and the catecholamines adrenaline/noradrenaline are responsible for signalling a wide range of processes involved in cell survival, cell cycle and immune function. Synthetic GCs are also often prescribed as co-medication alongside chemotherapy, and increasing evidence suggests that GCs may induce chemoresistance in multiple cancer types. In this review, we bring together evidence linking psychological stress hormone signalling with resistance to chemo- and immune therapies, as well as mechanistic evidence regarding the effects of exogenous stress hormones on the efficacy of chemotherapies.

摘要

被诊断患有癌症的患者常常会经历相当大的心理困扰,而心理应激反应的诱导与化疗反应不佳有关。心理应激反应由糖皮质激素(GCs)和儿茶酚胺的波动介导。GCs以及儿茶酚胺肾上腺素/去甲肾上腺素与它们各自的受体结合,负责发出涉及细胞存活、细胞周期和免疫功能的广泛过程的信号。合成GCs也经常作为辅助药物与化疗一起使用,越来越多的证据表明GCs可能在多种癌症类型中诱导化疗耐药性。在这篇综述中,我们汇集了将心理应激激素信号与化疗和免疫治疗耐药性联系起来的证据,以及关于外源性应激激素对化疗疗效影响的机制证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/046e37279676/cdr-2-773.fig.4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/c535d35c18ee/cdr-2-773.fig.1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/687534a04fae/cdr-2-773.fig.2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/7fd20e9e034f/cdr-2-773.fig.3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/046e37279676/cdr-2-773.fig.4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/c535d35c18ee/cdr-2-773.fig.1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/687534a04fae/cdr-2-773.fig.2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/7fd20e9e034f/cdr-2-773.fig.3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8992509/046e37279676/cdr-2-773.fig.4.jpg

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β-Adrenergic Signaling in Mice Housed at Standard Temperatures Suppresses an Effector Phenotype in CD8 T Cells and Undermines Checkpoint Inhibitor Therapy.
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