Targeted reactivation of the novel tumor suppressor DAPK1, an upstream regulator of p53, in high-grade serous ovarian cancer by mRNA liposomes reduces viability and enhances drug sensitivity in preclinical models.

IF 20.1 1区医学 Q1 ONCOLOGY

Cancer Communications Pub Date : 2025-05-20 DOI:10.1002/cac2.70029

Monika Raab, Balázs Győrffy, Samuel Peña-Llopis, Daniela Fietz, Monika Kressin, Margareta Kolaric, Matthias Ebert, Khayal Gasimli, Sven Becker, Mourad Sanhaji, Klaus Strebhardt

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在临床前模型中，新型肿瘤抑制因子DAPK1 （p53的上游调节因子）在高级别浆液性卵巢癌中通过mRNA脂质体靶向再激活，可降低生存能力并增强药物敏感性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cancer Communications Biochemistry, Genetics and Molecular Biology-Cancer Research

CiteScore

25.50

自引率

4.30%

发文量

153

审稿时长

4 weeks

期刊介绍： Cancer Communications is an open access, peer-reviewed online journal that encompasses basic, clinical, and translational cancer research. The journal welcomes submissions concerning clinical trials, epidemiology, molecular and cellular biology, and genetics.