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Additional file 5: Figure S3. E-cadherin (left) and HER2 expression in metastatic, moderately to poorly differentiated adenocarcinoma of the stomach SB.msgc-1. Immunohistochemical staining at magnification Ă 20, inlet Ă 40.

Additional file 6: Figure S4. Diagrams of different dose responses and the corresponding curve response class (CRC) scores. CRC parameters integrate potency and efficacy measurements of the compounds. Drug response curves with CRC −1.1 exhibit a near complete maximum response; −1.2 exhibit less effective maximum cell killing; −2.1 do not have a maximum response but can achieve killing of nearly all the cells; −2.2 do not have a maximum response and can only achieve intermediate killing; and 4 are inactive.

Additional file 3: Figure S1. Protein product of c.1380delA CDH1 variant predicted by MutationTaster. Wild type CDH1 sequence (UniProt ENST00000261769) shown on top, c.1380delA CDH1 variant on bottom.

Additional file 9: Figure S7. Increased induced cell death upon treatment with topoisomerase II and dual PI3K/mTOR in hereditary c.1380delA CDH1 SB.mhdgc-1 versus sporadic gastric cancer cell lines. Caspase 3/7 levels after 24 h of treatment with 1 µM mitoxantrone, 1 µM etoposide, or 1 µM PI-103 normalized to DMSO-treated control is shown (standard errors of the mean from at least 2 independent experiments done in triplicate shown).

Additional file 5: Figure S3. E-cadherin (left) and HER2 expression in metastatic, moderately to poorly differentiated adenocarcinoma of the stomach SB.msgc-1. Immunohistochemical staining at magnification Ă 20, inlet Ă 40.

Additional file 4: Figure S2. Top ten Gene Ontology (GO) cellular processes differently regulated in c.1380delA CDH1 SB.mhdgc-1 versus panel of sporadic gastric cancer cells. Enrichment analysis of all genes with FC > 2; p

Additional file 8: Figure S6. A, Target enrichment for compounds with CRC −1.1, −1.2, −2.1, or −2.2 and delta logAC50 (SB.mhdgc-1 logAC50–SB.msgc-1 logAC50) < −1. −log p values were calculated as described in materials and methods based on the total number of compounds targeting a gene or mechanism. B, LogAC50 distributions of compounds that show CRC −1.1, −1.2, −2.1, or −2.1 and logAC50

Additional file 6: Figure S4. Diagrams of different dose responses and the corresponding curve response class (CRC) scores. CRC parameters integrate potency and efficacy measurements of the compounds. Drug response curves with CRC −1.1 exhibit a near complete maximum response; −1.2 exhibit less effective maximum cell killing; −2.1 do not have a maximum response but can achieve killing of nearly all the cells; −2.2 do not have a maximum response and can only achieve intermediate killing; and 4 are inactive.

Additional file 8: Figure S6. A, Target enrichment for compounds with CRC −1.1, −1.2, −2.1, or −2.2 and delta logAC50 (SB.mhdgc-1 logAC50–SB.msgc-1 logAC50) < −1. −log p values were calculated as described in materials and methods based on the total number of compounds targeting a gene or mechanism. B, LogAC50 distributions of compounds that show CRC −1.1, −1.2, −2.1, or −2.1 and logAC50

Additional file 1: Table S1. Chromosomal aberrations detected by FISH in SB.mhdgc-1.

Additional file 4: Figure S2. Top ten Gene Ontology (GO) cellular processes differently regulated in c.1380delA CDH1 SB.mhdgc-1 versus panel of sporadic gastric cancer cells. Enrichment analysis of all genes with FC > 2; p

Additional file 7: Figure S5. Selective pharmacological vulnerabilities of c.1380delA SB.mhdgc-1 versus SB.msgc-1 gastric cancer cells identified by comparative qHTS screening with the MIPE Oncology 4.0 library. A, Bubble diagram of drug phenotypes by compound class of SB.mhdgc-1 versus SB.msgc-1 cells depicting class activities (number of compounds per drug class) measured by maximum response (max response SB.mhdgc-1 / max response SB.msgc-1). B, Bubble diagram comparing drug activities measured by potency (logAC50SB.mhdgc-1 versus logAC50SB.msgc-1).

Additional file 9: Figure S7. Increased induced cell death upon treatment with topoisomerase II and dual PI3K/mTOR in hereditary c.1380delA CDH1 SB.mhdgc-1 versus sporadic gastric cancer cell lines. Caspase 3/7 levels after 24 h of treatment with 1 µM mitoxantrone, 1 µM etoposide, or 1 µM PI-103 normalized to DMSO-treated control is shown (standard errors of the mean from at least 2 independent experiments done in triplicate shown).

Additional file 1: Table S1. Chromosomal aberrations detected by FISH in SB.mhdgc-1.

Additional file 3: Figure S1. Protein product of c.1380delA CDH1 variant predicted by MutationTaster. Wild type CDH1 sequence (UniProt ENST00000261769) shown on top, c.1380delA CDH1 variant on bottom.

Additional file 7: Figure S5. Selective pharmacological vulnerabilities of c.1380delA SB.mhdgc-1 versus SB.msgc-1 gastric cancer cells identified by comparative qHTS screening with the MIPE Oncology 4.0 library. A, Bubble diagram of drug phenotypes by compound class of SB.mhdgc-1 versus SB.msgc-1 cells depicting class activities (number of compounds per drug class) measured by maximum response (max response SB.mhdgc-1 / max response SB.msgc-1). B, Bubble diagram comparing drug activities measured by potency (logAC50SB.mhdgc-1 versus logAC50SB.msgc-1).