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程序性细胞死亡破坏炎症性肿瘤微环境(TME)并促进胶质母细胞瘤的演变。

Programmed cell death disrupts inflammatory tumor microenvironment (TME) and promotes glioblastoma evolution.

机构信息

Department of Neurosurgery, Center for Malignant Brain Tumors, National Glioma MDT Alliance, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.

'4+4' Medical Doctor Program, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.

出版信息

Cell Commun Signal. 2024 Jun 18;22(1):333. doi: 10.1186/s12964-024-01602-0.

DOI:10.1186/s12964-024-01602-0
PMID:38890642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11184850/
Abstract

Glioblastoma (GBM) is the most common malignant brain tumor and has a dismal prognosis even under the current first-line treatment, with a 5-year survival rate less than 7%. Therefore, it is important to understand the mechanism of treatment resistance and develop new anti-tumor strategies. Induction of programmed cell death (PCD) has become a promising anti-tumor strategy, but its effectiveness in treating GBM remains controversial. On the one hand, PCD triggers tumor cell death and then release mediators to draw in immune cells, creating a pro-inflammatory tumor microenvironment (TME). One the other hand, mounting evidence suggests that PCD and inflammatory TME will force tumor cells to evolve under survival stress, leading to tumor recurrence. The purpose of this review is to summarize the role of PCD and inflammatory TME in the tumor evolution of GBM and promising methods to overcome tumor evolution.

摘要

胶质母细胞瘤(GBM)是最常见的恶性脑肿瘤,即使在当前的一线治疗下,预后也很差,5 年生存率低于 7%。因此,了解治疗耐药的机制并开发新的抗肿瘤策略非常重要。程序性细胞死亡(PCD)的诱导已成为一种有前途的抗肿瘤策略,但它在治疗 GBM 中的有效性仍存在争议。一方面,PCD 引发肿瘤细胞死亡,然后释放介质吸引免疫细胞,形成促炎的肿瘤微环境(TME)。另一方面,越来越多的证据表明,PCD 和炎症性 TME 将迫使肿瘤细胞在生存压力下进化,导致肿瘤复发。本综述的目的是总结 PCD 和炎症性 TME 在 GBM 肿瘤进化中的作用以及克服肿瘤进化的有前途的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3352/11184850/2d3cdd7475dd/12964_2024_1602_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3352/11184850/01a523c7706c/12964_2024_1602_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3352/11184850/2d3cdd7475dd/12964_2024_1602_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3352/11184850/01a523c7706c/12964_2024_1602_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3352/11184850/2d3cdd7475dd/12964_2024_1602_Fig2_HTML.jpg

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