Comparison of nilotinib and imatinib inhibition of FMS receptor signaling, macrophage production and osteoclastogenesis

@article{Brownlow2008ComparisonON,
  title={Comparison of nilotinib and imatinib inhibition of FMS receptor signaling, macrophage production and osteoclastogenesis},
  author={Nicola Brownlow and Alexandra E. Russell and H Saravanapavan and Marion Wiesmann and James Murray and Paul W. Manley and N J Dibb},
  journal={Leukemia},
  year={2008},
  volume={22},
  pages={649-652}
}
Comparison of nilotinib and imatinib inhibition of FMS receptor signaling, macrophage production and osteoclastogenesis 
Tandutinib inhibits FMS receptor signalling, and macrophage and osteoclast formation in vitro
Tandutinib inhibits FMS receptor signalling, and macrophage and osteoclast formation in vitro
Second-generation TKI dasatinib inhibits proliferation of mesenchymal stem cells and osteoblast differentiation in vitro
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Second-generation TKI dasatinib inhibits proliferation of mesenchymal stem cells and osteoblast differentiation in vitro and prevents cell reprograming in vitro. Expand
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It is reported that platelet-derived growth factor receptor beta (PDGFR β) signaling regulates OPG production in vitro and that TKIs have effects on RANKL signaling through inhibition of the PDGFRβ and other target receptors. Expand
The skeletal effects of the tyrosine kinase inhibitor nilotinib.
TLDR
In 10 patients receiving nilotinib, levels of bone turnover markers were in the low-normal range, despite secondary hyperparathyroidism, findings that are similar to those in patients treated with imatinib, suggesting thatnilotinib may have important effects on bone metabolism. Expand
Comparative suppressive effects of tyrosine kinase inhibitors imatinib and nilotinib in models of autoimmune arthritis
TLDR
It is suggested that Imatinib and nilotinib could prevent autoimmune arthritis, essentially via distinct mechanisms, in that imatinib inhibits both inflammatory and T-cell-derived cytokine production, whereasnilotinib suppresses T- cell-derivedocyte proliferation. Expand
Comparative suppressive effects of tyrosine kinase inhibitors imatinib and nilotinib in models of autoimmune arthritis
Abstract Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint clusterExpand
Dysregulation of bone remodeling by imatinib mesylate.
TLDR
Recent studies suggesting that imatinib has direct effects on bone-resorbing osteoclasts and bone-forming osteoblasts through inhibition of c-fms, c-kit, carbonic anhydrase II, and the platelet-derived growth factor receptor are examined. Expand
Comparative suppressive effects of tyrosine kinase inhibitors imatinib and nilotinib in models of autoimmune arthritis
TLDR
It is suggested that Imatinib and nilotinib could prevent autoimmune arthritis, essentially via distinct mechanisms, in that imatinib inhibits both inflammatory and T-cell-derived cytokine production, whereasnilotinib suppresses T- cell-derived IL-17 production. Expand
Colony stimulating factor-1 receptor as a target for small molecule inhibitors.
TLDR
Five small molecule inhibitors of type III receptor tyrosine kinases were evaluated for binding to the closely related receptor, FMS, by docking into models of inactive and active conformations of the FMS kinase domain to confirm the docking predictions. Expand
BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?
TLDR
Clinical data has guided mechanistic studies toward alteration of platelet functions and atherosclerosis development, which might be secondary to metabolism impairment, suggesting a potentially protecting cardiovascular effect of this treatment in patients with BCR-ABL CML. Expand
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