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靶向细胞周期蛋白依赖性激酶2以对抗癌症治疗中的耐药性。

Targeting CDK2 to combat drug resistance in cancer therapy.

作者信息

Kasirzadeh Sara, Lenjisa Jimma Likisa, Wang Shudong

机构信息

Drug Discovery & Development, Clinical & Health Sciences, University of South Australia, Adelaide, 5000, Australia.

出版信息

Future Oncol. 2024 Dec;20(39):3325-3341. doi: 10.1080/14796694.2024.2416382. Epub 2024 Oct 29.

DOI:10.1080/14796694.2024.2416382
PMID:39469865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11633421/
Abstract

Drug resistance remains a major obstacle in cancer treatment, leading to treatment failures and high mortality rates. Despite advancements in therapies, overcoming resistance requires a deeper understanding of its mechanisms. This review highlights CDK2's pivotal role in both intrinsic and acquired resistance, and its potential as a therapeutic target. Cyclin E upregulation, which partners with CDK2, is linked to poor prognosis and resistance across various cancers. Specifically, amplifications of are associated with resistance to targeted therapies, immunotherapy, endocrine therapies and chemo/radiotherapy. Given CDK2's involvement in resistance mechanisms, investigating its role presents promising opportunities for developing novel strategies to combat resistance and improve treatment outcomes.

摘要

耐药性仍然是癌症治疗中的一个主要障碍,导致治疗失败和高死亡率。尽管治疗方法有所进步,但克服耐药性需要更深入地了解其机制。本综述强调了CDK2在固有耐药性和获得性耐药性中的关键作用及其作为治疗靶点的潜力。与CDK2协同作用的细胞周期蛋白E上调与多种癌症的不良预后和耐药性相关。具体而言,[此处原文缺失具体内容]的扩增与对靶向治疗、免疫治疗、内分泌治疗和化疗/放疗的耐药性有关。鉴于CDK2参与耐药机制,研究其作用为开发对抗耐药性和改善治疗结果的新策略提供了有前景的机会。

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