文章：

弥漫性胶质瘤伴FGFR3-TACC3融合：致癌机制、特征与治疗前景

Diffuse Gliomas with FGFR3-TACC3 Fusions: Oncogenic Mechanisms, Hallmarks, and Therapeutic Perspectives

原文发布日期：23 November 2023

DOI: 10.3390/cancers15235555

类型: Article

开放获取: 是

英文摘要：

In 2012, whole-transcriptome sequencing analysis led to the discovery of recurrent fusions involving theFGFR3andTACC3genes as the main oncological driver in a subset of human glioblastomas. Since then,FGFR3-TACC3fusions have been identified in several other solid cancers. Further studies dissected the oncogenic mechanisms of the fusion protein and its complex interplay with cancer cell metabolism.FGFR3-TACC3fusion-driven gliomas emerged as a defined subgroup with specific clinical, histological, and molecular features. SeveralFGFRinhibitors were tested inFGFR3-TACC3fusion-positive gliomas and proved some efficacy, although inferior to the results seen in otherFGFR3-TACC3fusion-driven cancers. In this review, we summarize and discuss the state-of-the-art knowledge resulting from a 10-year research effort in the field, its clinical implications for glioma patients, the potential reasons for targeted therapy failures, and the perspective of emerging treatments.

摘要翻译： 

2012年，全转录组测序分析发现，在部分人类胶质母细胞瘤中存在以FGFR3和TACC3基因融合为主要致癌驱动因素的现象。此后，FGFR3-TACC3融合在其他多种实体瘤中也得到确认。进一步研究揭示了该融合蛋白的致癌机制及其与癌细胞代谢的复杂相互作用。FGFR3-TACC3融合驱动的胶质瘤已形成一个具有特定临床、组织学和分子特征的明确亚群。多种FGFR抑制剂已在FGFR3-TACC3融合阳性胶质瘤中进行测试，虽显示出一定疗效，但效果逊于其他FGFR3-TACC3融合驱动的癌症。本综述系统总结并讨论了该领域十年研究积累的前沿认知，及其对胶质瘤患者的临床意义、靶向治疗失败的潜在原因，以及新兴治疗策略的发展前景。

原文链接：

Diffuse Gliomas with FGFR3-TACC3 Fusions: Oncogenic Mechanisms, Hallmarks, and Therapeutic Perspectives