原肌球蛋白受体激酶B (TrkB)信号传导:神经源性肿瘤的靶向治疗

IF 3.4 2区医学 Q1 PATHOLOGY

Journal of Pathology Clinical Research Pub Date : 2022-12-19 DOI:10.1002/cjp2.307

Yuehua Li, Chengjiang Wei, Wei Wang, Qingfeng Li, Zhi-Chao Wang

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引用次数: 2

摘要

原肌球蛋白受体激酶B (TrkB)是一种跨膜受体蛋白，在神经发育中起关键作用。该蛋白由神经营养受体酪氨酸激酶2 (NTRK2)基因编码，在多种类型的神经源性肿瘤中，由NTRK2过表达或融合引起的异常激活可促进肿瘤的发生、进展和对治疗的抵抗。针对这一机制的靶向治疗已经在临床前和临床研究中被设计和开发，包括选择性TrkB抑制剂和泛trk抑制剂。本文综述了TrkB在神经源性肿瘤中的基因结构、生物学功能、异常激活机制以及目前相关的靶向治疗方法。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Tropomyosin receptor kinase B (TrkB) signalling: targeted therapy in neurogenic tumours

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Tropomyosin receptor kinase B (TrkB) signalling: targeted therapy in neurogenic tumours

Tropomyosin receptor kinase B (TrkB), a transmembrane receptor protein, has been found to play a pivotal role in neural development. This protein is encoded by the neurotrophic receptor tyrosine kinase 2 (NTRK2) gene, and its abnormal activation caused by NTRK2 overexpression or fusion can contribute to tumour initiation, progression, and resistance to therapeutics in multiple types of neurogenic tumours. Targeted therapies for this mechanism have been designed and developed in preclinical and clinical studies, including selective TrkB inhibitors and pan-TRK inhibitors. This review describes the gene structure, biological function, abnormal TrkB activation mechanism, and current-related targeted therapies in neurogenic tumours.

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来源期刊

Journal of Pathology Clinical Research Medicine-Pathology and Forensic Medicine

CiteScore

7.40

自引率

2.40%

发文量

审稿时长

20 weeks

期刊介绍： The Journal of Pathology: Clinical Research and The Journal of Pathology serve as translational bridges between basic biomedical science and clinical medicine with particular emphasis on, but not restricted to, tissue based studies. The focus of The Journal of Pathology: Clinical Research is the publication of studies that illuminate the clinical relevance of research in the broad area of the study of disease. Appropriately powered and validated studies with novel diagnostic, prognostic and predictive significance, and biomarker discover and validation, will be welcomed. Studies with a predominantly mechanistic basis will be more appropriate for the companion Journal of Pathology.