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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: Transcriptomic profiling and quantitative high-throughput (qHTS) drug screening of CDH1 deficient hereditary diffuse gastric cancer (HDGC) cells identify treatment leads for familial gastric cancer

Fig. 5

c.1380 CDH1 SB.mhdgc-1 gastric cancer cells show vulnerabilities to toposisomerase II and PI3K/mTOR inhibition. a Drug response curves of a panel of gastric cancer cell lines treated with a range of concentrations of mitoxantrone, etoposide (both TOPO2A inhibitors), or PI-103 (dual class IA phosphatidylinositol 3 kinase/mTOR inhibitor) for 72 h. X-axis indicates log [concentration] tested, y-axis indicates cell viability percentage normalized to vehicle-control samples. Mean cell viability values are plotted with standard error of the mean (SEM) from at least 2 independent experiments done in triplicate. b Rate of apoptosis induced by 24-h treatment of 1 µM etoposide, mitoxantrone, or PI-103 normalized to DMSO-treated samples in sporadic gastric cancer SNU-16 and hereditary c.1380delA SB.mhdgc-1 cells. Flow cytometry profiles of FITC-labeled anti-BrdU staining of 3′-hydroxyl (OH) termini of double- and single-stranded DNA, relative BrdU fractions normalized to DMSO-treated control shown on the right

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