Supplemental Figure 1 from CTLA-4 Blockade Synergizes Therapeutically with PARP Inhibition in BRCA1-Deficient Ovarian Cancer

Treatment diagram for the combination therapy protocol.</p

Supplemental Figure 3 from CTLA-4 Blockade Synergizes Therapeutically with PARP Inhibition in BRCA1-Deficient Ovarian Cancer

PARP inhibition and CTLA-4 mAb combination therapy is ineffective against a BRCAwt cancer.</p

Supplemental Figure 2 from CTLA-4 Blockade Synergizes Therapeutically with PARP Inhibition in BRCA1-Deficient Ovarian Cancer

Combined treatment with the PARP-inhibitor and CTLA-4 antibody is effective in an orthotopic tumor model.</p

Toward the Development of a Potent and Selective Organoruthenium Mammalian Sterile 20 Kinase Inhibitor

Mammalian sterile 20 (MST1) kinase, a member of the sterile 20 (Ste-20) family of proteins, is a proapoptotic cytosolic kinase that plays an important role in the cellular response to oxidative stress. In this study, we report on the development of a potent and selective MST1 kinase inhibitor based on a ruthenium half-sandwich scaffold. We show that the enantiopure organoruthenium inhibitor, 9E1, has an IC50 value of 45 nM for MST1 and a greater than 25-fold inhibitor selectivity over the related Ste-20 kinases, p21 activated kinase 1 (PAK1), and p21 activated kinase 4 (PAK4) and an almost 10-fold selectivity over the related thousand-and-one amino acids kinase 2 (TAO2). Compound 9E1 also displays a promising selectivity profile against unrelated protein kinases; however, the proto-oncogene serine/threonine protein kinase PIM1 (PIM-1) and glycogen synthase kinase 3 (GSK-3β) are inhibited with IC50 values in the low nanomolar range. We also show that 9E1 can inhibit MST1 function in cells. A cocrystal structure of a related compound with PIM-1 and a homology model with MST1 reveals the binding mode of this scaffold to MST1 and provides a starting point for the development of improved MST1 kinase inhibitors for possible therapeutic application

Supplementary Fig. S2 from CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model

Supplementary Fig. S2 from CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine mode

Supplemental Table S1 from <i>DNMT3A</i> Mutational Status Affects the Results of Dose-Escalated Induction Therapy in Acute Myelogenous Leukemia

Supplemental Table S1. Frequency of DNMT3A mutations</p

Supplementary Table S1 from CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model

Supplementary Table S1 from CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine mode

Supplemental Figure S1 from <i>DNMT3A</i> Mutational Status Affects the Results of Dose-Escalated Induction Therapy in Acute Myelogenous Leukemia

Supplemental Figure S1. Patient flow diagram</p

Supplementary Fig. S1 from CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model

Supplementary Fig. S1 from CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine mode

Supplemental Figure S2 from <i>DNMT3A</i> Mutational Status Affects the Results of Dose-Escalated Induction Therapy in Acute Myelogenous Leukemia

Supplemental Figure S2. Circos diagram of concurrent mutations in the 152 patient cohort</p