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克唑替尼减少了神经纤维瘤化疗过程中的听力损伤

2018-02-26 MedSci MedSci原创

克唑替尼神经纤维瘤听力损伤
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克唑替尼是由辉瑞公司研制的抑制MET/ALK/ROS的ATP竞争性的多靶点蛋白激酶抑制剂，分别在ALK、ROS和MET激酶活性异常的肿瘤患者中证实克唑替尼对人体有显著临床疗效。将肿瘤靶向治疗药物克唑替尼加入到遗传性神经纤维瘤（NF2）的放射疗法中可以减少放射疗法导致的听力损伤。

克唑替尼是由辉瑞公司研制的抑制MET/ALK/ROS的ATP竞争性的多靶点蛋白激酶抑制剂，分别在ALK、ROS和MET激酶活性异常的肿瘤患者中证实克唑替尼对人体有显著临床疗效。将肿瘤靶向治疗药物克唑替尼加入到遗传性神经纤维瘤（NF2）的放射疗法中可以减少放射疗法导致的听力损伤。

麻省总医院（MGH）的研究小组报告称，使用克唑替尼阻断特定的分子途径，能够增强NF2小鼠模型对放射性疗法的敏感性，从而减少放射剂量，并抑制体外培养的NF2肿瘤细胞的生长。对于大多数神经纤维瘤患者而言，听力损伤是这些肿瘤中失能最严重的症状，而肿瘤主要治疗手段 - 放疗和手术 - 可能进一步损害听力。这就迫切需要开发一种既能增加治疗效果又能减少相关性听力损坏的新型治疗策略。

在两种小鼠模型中，使用克唑替尼阻断HGF-cMET途径能够增强辐射诱导的DNA损伤，显著减少了肿瘤生长。 cMET的基因敲除同样具有相似的结果，并且使用新型小鼠模型的实验显示阻断cMET本身不会影响动物的听力。 

原始出处：

https://www.europeanpharmaceuticalreview.com/news/72461/crizotinib-radiation-therapy-nf2/

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    2018-02-28 ms3046638856685384

    #损伤#

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    2018-02-28 stfoxst

    #神经纤维#

    0

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ALK阳性的晚期NSCLC患者可以从ALK抑制剂的治疗中显着获益，然而，不同患者的获益不一。既往的研究提示，ALK变体亚型可能影响患者接受ALK抑制剂治疗的疗效，但其背后的生物学机理尚未明确。近日，《JCO》发布的一项研究，通过对ALK不同变体患者耐药机制的探索，寻找答案。