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Receptor tyrosine kinases (RTKs) regulate cell proliferation, survival, migration, and differentiation through tyrosine phosphorylation. RTK mutations, amplifications, fusions, or abnormal expression can continuously activate MAPK, PI3K/AKT, STAT, PLC, and other signaling pathways, thereby ...
受体酪氨酸激酶（receptor tyrosine kinase，RTK）通过酪氨酸磷酸化调控细胞增殖、存活、迁移和分化。RTK突变、扩增、融合或异常表达可持续激活MAPK、PI3K/AKT、STAT和PLC等信号通路，推动肿瘤发生并影响分子分型、靶向治疗及耐药。
Non-small cell lung cancer exhibits substantial histological and molecular heterogeneity. Alterations involving EGFR, ALK, ROS1, KRAS, BRAF, RET, MET, HER2, and other oncogenic drivers can continuously activate tumor-cell proliferation and survival signaling and generate molecular subtypes with ...
非小细胞肺癌具有显著的组织学和分子异质性。EGFR、ALK、ROS1、KRAS、BRAF、RET、MET和HER2等异常可持续激活肿瘤细胞增殖与存活信号，并形成具有不同生物学特征和药物敏感性的分子亚型。
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