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胶质母细胞瘤中的辐射诱导衰老:机制与根除策略概述

Radiation-induced senescence in glioblastoma: An overview of the mechanisms and eradication strategies.

作者信息

Dehghan Neda, Mousavikia Seyedeh Nasibeh, Qasempour Younes, Azimian Hosein

机构信息

Department of Medical Physics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Department of Medical Physics, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Medical Physics Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.

出版信息

Life Sci. 2024 Dec 15;359:123218. doi: 10.1016/j.lfs.2024.123218. Epub 2024 Nov 5.

Abstract

Radiotherapy as a treatment method for glioblastoma is limited due to the intrinsic apoptosis resistance mechanisms of the tumor. Administration of higher radiation doses contributes to toxicities in normal tissues and organs at risk, like optic chiasma. Cellular senescence represents an alternative mechanism to apoptosis following radiotherapy in glioblastoma, occurring in both normal and neoplastic cells. Although it impedes the growth of tumors and sustains cells in their cycle, it can also act as a cause of tumor development and recurrence following treatment. In this review, we discuss detailed insights into the significance of radiation-induced senescence in glioblastoma and the underlying mechanisms that lead to radioresistance. We also discuss senescence biomarkers and the role of senescence-associated secretory phenotype (SASP) in tumor recurrence. Finally, we review the studies that have administered potential interventions to eradicate or inhibit senescent cells in glioblastoma after treatment with radiation.

摘要

由于肿瘤固有的抗凋亡机制,放射疗法作为胶质母细胞瘤的一种治疗方法受到限制。给予更高的辐射剂量会导致正常组织和高危器官(如视交叉)出现毒性。细胞衰老代表了胶质母细胞瘤放疗后凋亡的一种替代机制,在正常细胞和肿瘤细胞中均会发生。虽然它会阻碍肿瘤生长并使细胞维持在细胞周期中,但它也可能成为治疗后肿瘤发展和复发的一个原因。在这篇综述中,我们详细讨论了辐射诱导的衰老在胶质母细胞瘤中的意义以及导致放射抗性的潜在机制。我们还讨论了衰老生物标志物以及衰老相关分泌表型(SASP)在肿瘤复发中的作用。最后,我们回顾了那些在放疗后给予潜在干预措施以根除或抑制胶质母细胞瘤中衰老细胞的研究。

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