Ewing sarcoma (ES) is a rare, highly aggressive, bone, or soft tissue-associated tumor. Although this sarcoma often responds well to initial chemotherapy, 40% of the patients develop a lethal recurrence of the disease, with death recorded in 75–80% of patients with metastatic ES within 5 years, despite receiving high-dose chemotherapy. ES is genetically well-characterized, as indicated by the EWS-FLI1 fusion protein encoded as a result of chromosomal translocation in 80–90% of patients with ES, as well as in ES-related cancer cell lines. Recently, tyrosine kinases have been identified in the pathogenesis of ES. These tyrosine kinases, acting as oncoproteins, are associated with the clinical pathogenesis, metastasis, acquisition of self-renewal traits, and chemoresistance of ES, through the activation of various intracellular signaling pathways. This review describes the recent progress related to cellular and molecular functional roles of tyrosine kinases in the progression of ES.

尤文肉瘤 (ES) 是一种罕见的、高度侵袭性的骨或软组织相关肿瘤。尽管这种肉瘤通常对初始化疗反应良好，但 40% 的患者会出现致命的疾病复发，尽管接受了大剂量化疗，75-80% 的转移性 ES 患者仍会在 5 年内死亡。 ES 具有良好的遗传特征，80-90% 的 ES 患者以及 ES 相关癌细胞系中由于染色体易位而编码的 EWS-FLI1 融合蛋白表明了这一点。最近，酪氨酸激酶已被确定在 ES 的发病机制中。这些酪氨酸激酶作为癌蛋白，通过激活各种细胞内信号通路，与 ES 的临床发病机制、转移、自我更新特性的获得和化学耐药性相关。本综述描述了酪氨酸激酶在 ES 进展中的细胞和分子功能作用相关的最新进展。