A5099101361- Islamic Finance and Communication
- Mast cells and histamine
- Gastrointestinal Tumor Research and Treatment
- Synthesis and Catalytic Reactions
- Phosphodiesterase function and regulation
- Synthesis of β-Lactam Compounds
Otsuka (Japan)
2024
Abstract Purpose: Gastrointestinal stromal tumor (GIST), the most common mesenchymal with KIT or PDGFRA driver mutations, is typically treated tyrosine kinase inhibitors (TKI). However, resistance to TKIs due secondary mutations a challenge in advanced GISTs. In addition, there are currently no effective therapies for several other molecular subtypes, such as succinate dehydrogenase–deficient Therefore, novel therapeutic strategies needed. Experimental Design: To address this need, we tested...
<div>AbstractPurpose:<p>Gastrointestinal stromal tumor (GIST), the most common mesenchymal with <i>KIT</i> or <i>PDGFRA</i> driver mutations, is typically treated tyrosine kinase inhibitors (TKI). However, resistance to TKIs due secondary mutations a challenge in advanced GISTs. In addition, there are currently no effective therapies for several other molecular subtypes, such as succinate dehydrogenase–deficient Therefore, novel therapeutic strategies...
<p>Supplementary Fig. S3. Antagonistic effect of cilostamide on the anticancer activity OPB-171775</p>
<p>Supplementary Fig. S5. Flow cytometric analysis of cell cycle arrest and death induced by OPB-171775</p>
<p>Supplementary Fig. S5. Flow cytometric analysis of cell cycle arrest and death induced by OPB-171775</p>
<p>Supplementary Fig. S2. Coexpression of PDE3A and SLFN12 as sensitivity factors for OPB-171775</p>
<p>Supplementary Fig. S2. Coexpression of PDE3A and SLFN12 as sensitivity factors for OPB-171775</p>
<div>AbstractPurpose:<p>Gastrointestinal stromal tumor (GIST), the most common mesenchymal with <i>KIT</i> or <i>PDGFRA</i> driver mutations, is typically treated tyrosine kinase inhibitors (TKI). However, resistance to TKIs due secondary mutations a challenge in advanced GISTs. In addition, there are currently no effective therapies for several other molecular subtypes, such as succinate dehydrogenase–deficient Therefore, novel therapeutic strategies...
<p>Supplementary Fig. S1. PDE3A mRNA expression in PDX tumors and <i>in vivo</i> efficacy of OPB-171775</p>
<p>Supplementary Fig. S1. PDE3A mRNA expression in PDX tumors and <i>in vivo</i> efficacy of OPB-171775</p>
<p>Supplementary Fig. S3. Antagonistic effect of cilostamide on the anticancer activity OPB-171775</p>
<p>Supplementary Fig. S6. Effects of OPB-171775 on cell cycle and its combination with imatinib in GIST</p>
<p>Supplementary Fig. S4. GCN2 phosphorylation and downstream signaling induced by OPB-171775.</p>
<p>Supplementary Fig. S4. GCN2 phosphorylation and downstream signaling induced by OPB-171775.</p>
<p>Supplementary Fig. S6. Effects of OPB-171775 on cell cycle and its combination with imatinib in GIST</p>