With this in mind, we looked at the average SCNA profiles across small cohorts of patients with OAC, gastric adenocarcinoma (GAC) and BO (Supplementary Fig. S2, Methods), which highlighted amplifications of known oncogenes such as EGFR, MYC, GATA4, and MDM2, some with known drug targets, and deletions of tumour suppressor genes, e.g. FHIT, TP53, SMAD4 and RUNX1. This evidence concerns the gene RUNX1 and gastric adenocarcinoma.