摘要
肝细胞癌(HCC)是癌症相关死亡的第二大原因,其具有高发病率和较晚的早期诊断。酪氨酸激酶抑制剂(Tyrosine kinase inhibitors, TKIs)是一类小分子靶向药物,其临床疗效显著,临床不良反应发生率低,因此主要用于化疗后HCC的临床治疗。然而,耐药性对索拉非尼和其他可用于治疗晚期HCC的TKIs提出了一个重大挑战。最近的机制研究表明,上皮-间充质转化(EMT)、ATP结合盒(ABC)转运体、缺氧、自噬和血管生成参与了HCC患者的凋亡、血管生成、HCC细胞增殖和TKI耐药。探索和克服这种耐药机制对于提高TKI耐药的HCC患者的治疗效果至关重要。。本文旨在总结近年来提出的可能的耐药机制,以及在HCC背景下逆转TKI耐药的方法。
关键词: 肝细胞癌,酪氨酸激酶抑制剂,耐药机制,索拉非尼,靶蛋白,分子机制。
图形摘要
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