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Table 1 Drug sensitivities derived from in vitro models of HDGC

From: Merging perspectives: genotype-directed molecular therapy for hereditary diffuse gastric cancer (HDGC) and E-cadherin–EGFR crosstalk

  CDH1 MCF10A (−/−) [13] CDH1 MCF10A (−/−) [13] c.1380delA CDH1 HDGC [12] c.1380delA CDH1 HDGC [12]
qHTS drug phenotype Lethality by siRNA target or target ligand qHTS drug phenotype Target kinase in enriched top network
Drug class
 PI3K inhibitor Yes PIK3CA, PIK3CG, PIK3R5, PIK3CB, PIK3CD, PIK3C2B Yes No
 AKT1 No AKT1 No No
 mTOR inhibitor Yes   Yes Yes
 EGFR and PDGFR family inhibitor Yes PDGFD, EGFR, ERBB3, NRG1 No Yes
 Src kinase inhibitor Yes   No Yes
 FAK inhibitor ?   Yes Yes
 ALK/ROS1-like tyrosine  kinase inhibitor Yes ROS1, ALK Yes No
 JAK family inhibitor Yes JAK2 No No
 BCL2 inhibitor Yes BCL2 No No
 Aurora kinase inhibitor Yes   Yes No
 HDAC inhibitor Yes HDAC3, HDAC9, SIN3A, RERE No  
 ROCK inhibitor No   Yes No
 Protein kinase C inhibitor No   Yes Yes
  1. Quantitative high-throughput drug screening of MCF10A mammary epithelial cells vs isogenic CDH1−/− MCF10A cells and hereditary c.1380del CDH1 gastric cancer cells vs sporadic CDH1 wild type SB.msgc-1 cells. Listed are vulnerabilities selective in CDH1−/−-mutant MCF10A and c.1380del CDH1 cells, shared drug classes are highlighted in italics
  2. Active in both c.1380delA CDH1 mutant hereditary SB.mhdgc-1 and control CDH1 wild type SB.msgc-1 gastric cancer cells