Pub. Date : 2010 Sep
PMID : 20629553
10 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 2 | BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 3 | BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 4 | The objective of this study was to determine the effects of sunitinib on signal transduction pathways and on gene expression of iodide-metabolizing proteins in papillary cancer cells with the RET/PTC1 rearrangement. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 5 | RESULTS: Sunitinib inhibited proliferation of RET/PTC1 subclones in a time- and dose-related manner. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 6 | Incubation of RET/PTC1 cells with 1 microM sunitinib inhibited their migration potential and transformed their morphology. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 7 | Sunitinib inhibited RET autophosphorylation at Y1062 and the activation of signal transducer and activator of transcription 3 by blocking Y705 phosphorylation. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 8 | Sunitinib treatment of RET/PTC1 cell lines, in combination, with forskolin induced expression of the sodium (Na)/iodide (I) symporter (NIS) and the transcription factors that bind the NIS upstream enhancer. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 9 | CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells. | Sunitinib | ret proto-oncogene | Homo sapiens |
| 10 | CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells. | Sunitinib | ret proto-oncogene | Homo sapiens |