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衰老标志物阳性癌细胞的悖论:挑战与机遇

The paradox of senescent-marker positive cancer cells: challenges and opportunities.

作者信息

O'Sullivan Emily A, Wallis Ryan, Mossa Federica, Bishop Cleo L

机构信息

Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.

出版信息

NPJ Aging. 2024 Sep 14;10(1):41. doi: 10.1038/s41514-024-00168-y.

DOI:10.1038/s41514-024-00168-y
PMID:39277623
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11401916/
Abstract

Senescence is an anti-tumour mechanism and hallmark of cancer. Loss or mutation of key senescence effectors, such as p16INK4A, are frequently observed in cancer. Intriguingly, some human tumours are both proliferative and senescent-marker positive (Sen-Mark+). Here, we explore this paradox, focusing on the prognostic consequences and the current challenges in classifying these cells. We discuss future strategies for Sen-Mark+ cell detection together with emerging opportunities to exploit senescence for cancer.

摘要

衰老作为一种抗肿瘤机制,是癌症的一个标志。关键衰老效应因子(如p16INK4A)的缺失或突变在癌症中经常被观察到。有趣的是,一些人类肿瘤既具有增殖性又呈衰老标志物阳性(Sen-Mark+)。在此,我们探讨这一矛盾现象,重点关注其预后影响以及在对这些细胞进行分类时面临的当前挑战。我们讨论了Sen-Mark+细胞检测的未来策略以及利用衰老来治疗癌症的新机遇。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/8b612dfdc010/41514_2024_168_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/bac0874cf4f0/41514_2024_168_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/075b86f6e73a/41514_2024_168_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/565e14366c75/41514_2024_168_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/8b612dfdc010/41514_2024_168_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/bac0874cf4f0/41514_2024_168_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/075b86f6e73a/41514_2024_168_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/565e14366c75/41514_2024_168_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6296/11401916/8b612dfdc010/41514_2024_168_Fig4_HTML.jpg

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Integrative modeling uncovers p21-driven drug resistance and prioritizes therapies for PIK3CA-mutant breast cancer.
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Post-Translational Modifications of Proteins Orchestrate All Hallmarks of Cancer.蛋白质的翻译后修饰调控癌症的所有特征。
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