PDF file - 25K, Pharmacokinetic parameters of PKC412.

PDF file - 167KB, EGFR and PKCa are co-regulators of Aurora B kinase-mediated chromatin condensation in interphase.

Supplementary Figure 3 from Ligand-Dependent Platelet-Derived Growth Factor Receptor (PDGFR)-α Activation Sensitizes Rare Lung Cancer and Sarcoma Cells to PDGFR Kinase Inhibitors

Supplementary Figures 2-5 from Breast Tumor Kinase Phosphorylates p190RhoGAP to Regulate Rho and Ras and Promote Breast Carcinoma Growth, Migration, and Invasion

Supplementary Figure Legends 1-3, Table 1 from Elevated CRAF as a Potential Mechanism of Acquired Resistance to BRAF Inhibition in Melanoma

Suppl. Fig. 1-6. Fig. S1. Testing and optimization of short-term cell survival assays. S2. SRF2Gy measurements and correlations. S3. Analysis of apoptosis after drug/IR treatments. S4. Analysis of senescence after drug/IR treatments. S5. Radiosensitizing effects of everolimus. S6. Radiosensitzing effects of midostaurin.

Supplementary Figure S1. KP4-derived 3D spheroids with histopathological characteristics of micrometastases show differential sensitivity to small molecule inhibitors; Supplementary Figure S2. Cobimetinib/ponatinib co-treatment increases death of pancreatic cancer cells; Supplementary Figure S3. Cobimetinib/ponatinib co-treatment impairs tumor growth in KPP xenografts; Supplementary Table S1. List of small molecule inhibitors used in drug screen; Supplementary Table S2. Genotype with key mutations of cell lines used in this study; Supplementary Table S3. Tumor growth inhibition (%TGI) of KP4 and KPP xenografts; Supplementary Table S4. TCGA microarray data for normal and PDAC tissues

PDF file - 1635KB, Elevated ALDH1A1 activity in KATO II and GTL-16 DTPs (S1). ALDHhigh cells exhibit properties similar to CSCs (S2). Effect of DS on growth of parental cells and DTPs (S3). DS has opposite effects on pre- and post- KI-treated cells (S4). ALDH family members are expressed at higher level in DTPs (S5). Role of specific ALDH isoforms and cell density in drug tolerance drug (S6). Effect of the alternative ALDH inhibitor gossypol on drug-tolerant cells (S7). Increased mitochondrial respiration and ROS levels in KATO II ALDHhigh cells (S8). DS effect is not mediated by inhibition of efflux pumps or through proteasome inhibition (S9).

<p>Supplemental Figures S1-S11. Figure S1. AXL and GAS6 expression correlates with a mesenchymal signature. Figure S2. AXL staining in TNBC tissues samples. Figure S3. TGF-β-induced EMT is reversible, and TKI resistance upon EMT is not due to drug efflux. Figure S4. AXL inhibitor R428 suppresses GAS6-induced pAXL, downstream signaling and invasion capacity. Figure S5: Inhibition of AXL does not re-sensitize erlotinib-resistant cells. Figure S6: AXL over-expression or inhibition does not alter erlotinib sensitivity in the parental HCC827 cell line. Figure S7: Summary of Bliss scores and activity of MP-470, Erlotinib and Docetaxel (DTX) or combination treatment. Figure S8. R428 synergistically interacts with anti-mitotic agents and not with Doxorubicin or Cisplatin to reduce cell viability. Figure S9. AXL inhibition in combination with anti-mitotic agents promotes mitotic death. Figure S10. Suppression of pAKT, pS6 and pCDC2 following AXL inhibition. Figure S11: AXL knock-down increases p21 expression. Table S1. Mesenchymal PC9 cells are cross-resistant to a number of anti-cancer agents.</p>

Supplementary Figure 4 from Ligand-Dependent Platelet-Derived Growth Factor Receptor (PDGFR)-α Activation Sensitizes Rare Lung Cancer and Sarcoma Cells to PDGFR Kinase Inhibitors

XLSX file - 41KB, IC50 values for kinase inhibitors used in the study.

XLS file - 335KB, Gene expression comparison of KATO II cells and KATO II-derived DTPs.

Supplementary Figures 9-10 from Breast Tumor Kinase Phosphorylates p190RhoGAP to Regulate Rho and Ras and Promote Breast Carcinoma Growth, Migration, and Invasion

PDF file - 177K, Comparison of EGFR T790M inhibitors in NR6 cell lines expressing WT EGFR.

Supplementary Figure 5 from STAT3 Plays a Critical Role in KRAS-Induced Pancreatic Tumorigenesis

Supplementary Figure 3 from Elevated CRAF as a Potential Mechanism of Acquired Resistance to BRAF Inhibition in Melanoma