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在肺腺癌中,DSG2通过PTX3减弱了格姆西塔的疗效

Chin-Chou Wang1, Jo-Ying Lin2, Chih-Yang Wang3

  • 1Divisions of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan; Department of Respiratory Therapy, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan; Department of Internal Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, Taiwan.

Biochimica et biophysica acta. Molecular basis of disease
|May 2, 2025
PubMed
概括

在肺腺癌 (LUAD) 中,desmoglein 2 (DSG2) 的过度表达促进化学抵抗. 针对DSG2可以通过调节PTX3 / NFκB / STAT3通路来增强gemcitabine的疗效,从而提供针对LUAD的新策略.

关键词:
这是DSG2 DSG2耐药性 耐药性 耐药性 耐药性 耐药性肺部腺癌瘤是肺部腺癌.在 NFκBB 的情况下.PTX3PTX3PTX3 PTX3 PTX3 PTX3 PTX3 PTX3 PTX3 PTX3

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