Supplementary Tables 6 through 14 from Cell-Specific Computational Modeling of the PIM Pathway in Acute Myeloid Leukemia

The following tables are supplied in the excel file due to their sizes: Table S6. Phosphosite Overlap. PhosphoScan mass-spectrometry in MOLM16 cells after 3 hour treatment with AZD1208 Table S7. Literature Entries. Full literature entries. Table S8. Model Target Functions. Target functions for AML general model and cell specific calibrated AML model. Table S9. AML genotype state. Nodes settings for model initialization for each cell-specific state. Table S10. Immediate downstream effect of modelled AML genotypes. Direct modelled effect of each genotype. Table S11. Cell-specific AML network model replicates response to treatments reported in external publications. Summary of experimental conclusions compared to model predictions. Table S12. Combination strategy. showing predicted activity for combinations of PI3K inhibitor, AKT inhibitor, MEK inhibitor, and AKT inhibitor with the PIM inhibitor AZD1208 across the 4 AML cell lines. Table S13. MOLM16_Res_DNAseq. Whole exome DNA-seq for PIM inhibition resistant populations of MOLM16 cell line. Table S14. BIOGRID Interactions. BIOGRID interactions between putative resistant deriving genes to the RAS/PI3K and/or the AKT/MTOR signaling pathways.

以下表格因尺寸原因均提供于 Excel 文件中：
- 表 S6：磷酸位点重叠。在 MOLM16 细胞中经过 3 小时 AZD1208 处理后的 PhosphoScan 质谱分析。
- 表 S7：文献条目。完整的文献条目。
- 表 S8：模型目标函数。AML 通用模型及针对特定细胞校准的 AML 模型的目标函数。
- 表 S9：AML 基因型状态。针对每个细胞特异性状态的模型初始化的节点设置。
- 表 S10：模型预测的 AML 基因型的即时下游效应。每个基因型的直接模型效应。
- 表 S11：针对特定细胞的 AML 网络模型可复制外部出版物中报告的治疗反应。与模型预测相比的实验结论总结。
- 表 S12：联合策略。展示 PI3K 抑制剂、AKT 抑制剂、MEK 抑制剂与 PIM 抑制剂 AZD1208 在 4 种 AML 细胞系中组合预测的活性。
- 表 S13：MOLM16_Res_DNAseq。针对 MOLM16 细胞系中 PIM 抑制耐药群体的全外显子 DNA 测序。
- 表 S14：BIOGRID 交互作用。假设耐药基因与 RAS/PI3K 及/或 AKT/MTOR 信号通路之间的 BIOGRID 交互作用。