吉非替尼原发耐药与K-Ras突变及策略

  • 摘要: K-ras基因突变(mKRAS)可导致非小细胞肺癌(NSCLC)对表皮生长因子受体—酪氨酸激酶抑制剂(EGFR-TKI)原发耐药。由于KRAS通路的复杂性使其治疗成为目前热点及难点。以Ras信号通路为靶标的抗肿瘤治疗研究有可能克服EGFR-TKI原发耐药。本文就有关Ras及其通路上可能治疗靶点的研究进行综述。

     

    Abstract: K-Ras mutation ( mKRAS ) can result in the primary resistance of non-small cell lung carcinoma to epidermal growth factor receptor-tyrosine kinase inhibitor ( EGFR-TKI ). Due to the complexity of the KRAS pathway, the treatment of this condition has become the focus of interest and nodus of related studies. Anticancer treatments using the Ras signaling pathway as the target marker may overcome the primary resistance to EGFR-TKI. The possible targets of treatment using the Ras signaling pathway were reviewed in the present article.

     

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