选择性靶向AKT1 (E17K)突变:精准肿瘤学和治疗设计的进展

IF 2.9 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Xiaoyan Chen, Danfeng Zhang, Jiapeng Xue, Zhi Li
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引用次数: 0

摘要

AKT1 (E17K)突变与实体肿瘤的不良结果相关,促进癌症的增殖和持续。Gregory等人最近的一项研究发现了一种针对该突变的可逆共价抑制剂,具有显著的抗肿瘤作用,对正常细胞几乎没有影响。这一进展为akt突变型恶性肿瘤提供了靶向治疗方法,并为进一步的抑制剂研究提供了信息。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Selective targeting of the AKT1 (E17K) mutation: advances in precision oncology and therapeutic design.

The AKT1 (E17K) mutation, associated with unfavourable outcomes in solid tumours, promotes cancer proliferation and persistence. A recent study by Gregory et al. discovered a reversible covalent inhibitor targeting this mutation, exhibiting significant anti-tumor action with little effects on normal cells. This advancement provides a targeted therapeutic approach for AKT-mutant malignancies and informs further inhibitor research.

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来源期刊
Discover. Oncology
Discover. Oncology Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
2.40
自引率
9.10%
发文量
122
审稿时长
5 weeks
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