ARID1A-deficient Bladder Cancer is Dependent on PI3K Signaling, and can be Targeted via EZH2 and/or PI3K Pharmacologic Inhibition: Therapeutic Implications. ARID1A-deficient Bladder Cancer is Dependent on PI3K Signaling, and can be Targeted via EZH2 and/or PI3K Pharmacologic Inhibition: Therapeutic Implications

ARID1A-mutant bladder cancer is dependent on PI3K signaling and is sensitive to EZH2 and/or PI3K inhibition. Clinical trials in molecularly selected patients should be considered. Overall design: Cleavage Under Targets & Release Using Nuclease of RT112 cells in triplicate for ARID1A and H3K4me3

ARID1A突变型膀胱癌依赖PI3K信号通路，且对EZH2和/或PI3K抑制剂敏感，应考虑针对经分子筛选的患者开展相关临床试验。整体实验设计：对RT112细胞开展靶蛋白切割与核酸酶释放测序实验（Cleavage Under Targets & Release Using Nuclease，CUT&RUN），针对ARID1A与H3K4me3靶点设置三次生物学重复。