以脂质代谢为靶点克服弥漫大 B 细胞淋巴瘤对 BTK 抑制剂的耐药性

Q3 Medicine
Zhuojun Liu , Chenyue Wu , Zhaohua Yao , Yuxuan Wang , Zhe Yu , Jian Yu
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引用次数: 0

摘要

探索弥漫大 B 细胞淋巴瘤(DLBCL)的新型治疗靶点,以克服其对布鲁顿酪氨酸激酶(BTK)抑制剂的耐药性是一个关键课题。脂质代谢在各种癌症的耐药机制中至关重要,它可能会揭示 DLBCL 对 BTK 抑制剂耐药的新方面。尽管脂质代谢在肿瘤耐药模式中的重要性已众所周知,但它在DLBCL中的复杂作用及其对BTK抑制剂疗法的耐药性在很大程度上仍是未知数。本综述将探讨脂质代谢与 BTK 抑制剂耐药性之间的复杂关系,为提高 BTK 抑制剂的疗效和开发创新的 DLBCL 联合治疗方法提供新的见解。本综述有可能指导未来的研究方向,优化现有的治疗过程,并激励创新组合治疗策略的开发,从而改善 DLBCL 患者的预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting lipid metabolism overcomes BTK inhibitor resistance in diffuse large B-cell lymphoma

Exploring novel therapeutic targets of Diffuse large B cell lymphoma (DLBCL) to overcome its resistance to Bruton's Tyrosine Kinase (BTK) inhibitors is a key topic. Lipid metabolism, crucial in the resistance landscape of various cancers, may unlock new aspects of BTK inhibitor resistance in DLBCL. Despite the known importance of lipid metabolism in oncological resistance patterns, its intricate role in DLBCL and its resistance to BTK inhibitor therapies remains largely uncharted. This review will explore the complex relationship between lipid metabolism and BTK inhibitor resistance, giving new insights for improving the effectiveness of BTK inhibitors and developing innovative combination treatment methods for DLBCL. This review holds the potential for guiding future research directions, optimizing existing therapeutic processes, and inspiring the development of innovative combinatorial therapeutic strategies that improve outcomes in patients with DLBCL.

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来源期刊
Medicine in Novel Technology and Devices
Medicine in Novel Technology and Devices Medicine-Medicine (miscellaneous)
CiteScore
3.00
自引率
0.00%
发文量
74
审稿时长
64 days
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