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通过JAK-STAT激活,EML4-ALK融合驱动肺腺到状过渡

Zhen Qin1, Meiting Yue1,2, Shijie Tang1

  • 1State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences , Shanghai, China.

The Journal of experimental medicine
|January 29, 2024
PubMed
概括

ALK重组驱动肺癌的可塑性,使瘤细胞能够从腺癌转变为状细胞癌. 这种转变会产生耐药性,但与JAK抑制剂的联合治疗可能会克服这种转变.

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