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文章:

白血病中新细胞死亡机制的失调

Deregulation of New Cell Death Mechanisms in Leukemia

原文发布日期:25 April 2024

DOI: 10.3390/cancers16091657

类型: Article

开放获取: 是

 

英文摘要:

Hematological malignancies are among the top five most frequent forms of cancer in developed countries worldwide. Although the new therapeutic approaches have improved the quality and the life expectancy of patients, the high rate of recurrence and drug resistance are the main issues for counteracting blood disorders. Chemotherapy-resistant leukemic clones activate molecular processes for biological survival, preventing the activation of regulated cell death pathways, leading to cancer progression. In the past decade, leukemia research has predominantly centered around modulating the well-established processes of apoptosis (type I cell death) and autophagy (type II cell death). However, the development of therapy resistance and the adaptive nature of leukemic clones have rendered targeting these cell death pathways ineffective. The identification of novel cell death mechanisms, as categorized by the Nomenclature Committee on Cell Death (NCCD), has provided researchers with new tools to overcome survival mechanisms and activate alternative molecular pathways. This review aims to synthesize information on these recently discovered RCD mechanisms in the major types of leukemia, providing researchers with a comprehensive overview of cell death and its modulation.

 

摘要翻译: 

血液系统恶性肿瘤是全球发达国家中最常见的五种癌症之一。尽管新型治疗方法已显著改善患者的生活质量和预期寿命,但高复发率和耐药性仍是当前血液疾病治疗面临的主要挑战。化疗耐药的白血病克隆通过激活分子生物学存活机制,抑制程序性细胞死亡通路的启动,从而推动癌症进展。过去十年间,白血病研究主要聚焦于调控经典的细胞凋亡(I型细胞死亡)和自噬(II型细胞死亡)过程。然而,治疗耐药性的产生及白血病克隆的适应性进化,使得针对这些细胞死亡通路的靶向治疗策略逐渐失效。随着细胞死亡命名委员会对新型细胞死亡机制的界定与分类,研究人员获得了突破肿瘤存活机制、激活替代分子通路的新工具。本综述旨在系统阐述主要白血病类型中最新发现的程序性细胞死亡机制,为研究者提供关于细胞死亡及其调控策略的全面视角。

 

原文链接:

Deregulation of New Cell Death Mechanisms in Leukemia

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