在胰腺癌中,NFAT5控制了细胞可塑性驱动的对KRAS向治疗的耐药性

Daiyong Deng1,2, Habeebunnisa Begum1,2, Tong Liu1,2

  • 1Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers University New Jersey Medical School, Newark, NJ, USA.

概括

慢性胰腺炎通过TGFβ诱导的EMT促进胰腺癌中KRAS治疗的耐药性. 准核因子NFAT5 (激活T细胞的核因子5) 可以克服这种抵抗并提高生存率.

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