Fig. 6

Discovery of novel connections between two studies. a Venn diagram showing the number of metabolites common to both of the two studies on which P10-2[30] and P18-3 [38] were based. In both studies, metabolomic analyses were conducted using CE-TOFMS, GC–MS, and LC–MS. b Comparison of changes in the level of metabolites in P10-2 versus P18-3 (r = 0.656, p < 0.001, Spearman’s rank test). P10-2 represents the differential metabolomic profile in H1975 cells (H1975; human lung adenocarcinoma cell line) after treatment with PKI-587 (gedatolisib). P18-3 represents the metabolomic profile in L428 cells (L428; human Hodgkin’s lymphoma cell line) after treatment with tetra-O-methyl nordihydroguaiaretic acid (M4N). Their controls were the cells before drug treatment. In both nodes, the changes from control to drug-treated were calculated. Red plots represent metabolites found to be upregulated in the tumor group (treatment group), whereas blue plots represent those found to be downregulated. c A 2 × 2 contingency table of the numbers of upregulated and downregulated metabolites in the two nodes (log2 odds ratio = 4.81, p-value = 0.004). The table was created based on (b). See Fig. 2 for details on the table creation. d Schematic representation of PI3K/AKT/mTOR pathways and the point of inhibition by the drugs used in the two studies. Metabolite classifications to which simultaneously upregulated or downregulated metabolites belong are shown at the bottom. PI3K, phosphatidylinositol 3-kinase; PIP3, phosphatidylinositol 3-phosphate; PDK-1, 3-phosphoinositide-dependent protein kinase 1; Akt, protein kinase B (PKB, also called Akt); mTOR, mammalian target of rapamycin; Sp1, Specificity protein 1