The skeletal effects of the tyrosine kinase inhibitor nilotinib.

[1]  A. Branca,et al.  Effects of second‐generation tyrosine kinase inhibitors towards osteogenic differentiation of human mesenchymal cells of healthy donors , 2012, Hematological oncology.

[2]  He Huang,et al.  The tyrosine kinase inhibitor nilotinib inhibits proliferation and osteoblast differentiation of human mesenchymal stromal cells. , 2011, Bone.

[3]  J. Radich,et al.  Nilotinib is effective in patients with chronic myeloid leukemia in chronic phase after imatinib resistance or intolerance: 24-month follow-up results. , 2011, Blood.

[4]  Ricardo Pasquini,et al.  Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. , 2010, The New England journal of medicine.

[5]  J. Mestan,et al.  Extended kinase profile and properties of the protein kinase inhibitor nilotinib. , 2010, Biochimica et biophysica acta.

[6]  H. Joensuu,et al.  Nilotinib in the treatment of advanced gastrointestinal stromal tumours resistant to both imatinib and sunitinib. , 2009, European journal of cancer.

[7]  G. Gamble,et al.  Decreased bone turnover despite persistent secondary hyperparathyroidism during prolonged treatment with imatinib. , 2009, The Journal of clinical endocrinology and metabolism.

[8]  A. Chiarenza,et al.  Effects of imatinib mesylate in osteoblastogenesis. , 2009, Experimental hematology.

[9]  D. Mellström,et al.  Increased cortical bone mineralization in imatinib treated patients with chronic myelogenous leukemia , 2008, Haematologica.

[10]  M. Wiesmann,et al.  Comparison of nilotinib and imatinib inhibition of FMS receptor signaling, macrophage production and osteoclastogenesis , 2008, Leukemia.

[11]  S. Fitter,et al.  Long-term imatinib therapy promotes bone formation in CML patients. , 2008, Blood.

[12]  J. Cornish,et al.  Imatinib Promotes Osteoblast Differentiation by Inhibiting PDGFR Signaling and Inhibits Osteoclastogenesis by Both Direct and Stromal Cell‐Dependent Mechanisms , 2007, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[13]  G. Ehninger,et al.  Inhibition of platelet‐derived growth factor receptorβ by imatinib mesylate suppresses proliferation and alters differentiation of human mesenchymal stem cells in vitro , 2007, Cell proliferation.

[14]  I. Reid,et al.  The peroxisome proliferator-activated receptor-gamma agonist rosiglitazone decreases bone formation and bone mineral density in healthy postmenopausal women: a randomized, controlled trial. , 2007, The Journal of clinical endocrinology and metabolism.

[15]  J. Mestan,et al.  Identification of BCR-ABL point mutations conferring resistance to the Abl kinase inhibitor AMN107 (nilotinib) by a random mutagenesis study. , 2005, Blood.

[16]  I. Reid,et al.  The peroxisome proliferator-activated receptor-gamma agonist rosiglitazone decreases bone formation and bone mineral density in healthy postmenopausal women: a randomized, controlled trial. , 2007, The Journal of clinical endocrinology and metabolism.

[17]  I. Reid,et al.  Imatinib mesylate, increased bone formation, and secondary hyperparathyroidism. , 2006, The New England journal of medicine.

[18]  N. Sevenet,et al.  Imatinib mesylate (Gleevec) enhances mature osteoclast apoptosis and suppresses osteoclast bone resorbing activity. , 2006, European journal of pharmacology.

[19]  N. Sevenet,et al.  Ability of breast cancer cell lines to stimulate bone resorbing activity of mature osteoclasts correlates with an anti-apoptotic effect mediated by macrophage colony stimulating factor , 2006, Apoptosis.

[20]  S. Owen,et al.  Imatinib and altered bone and mineral metabolism. , 2006, The New England journal of medicine.

[21]  G. Lyritis,et al.  Imatinib and altered bone and mineral metabolism. , 2006, The New England journal of medicine.

[22]  K. Bhalla,et al.  Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. , 2006, The New England journal of medicine.

[23]  C. Peschel,et al.  The FIP1L1-PDGFRA T674I mutation can be inhibited by the tyrosine kinase inhibitor AMN107 (nilotinib). , 2006, Blood.

[24]  A. Zannettino,et al.  Imatinib as a potential antiresorptive therapy for bone disease. , 2006, Blood.

[25]  J. Mestan,et al.  AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL , 2006, British Journal of Cancer.

[26]  Glenn Heller,et al.  Altered bone and mineral metabolism in patients receiving imatinib mesylate. , 2006, The New England journal of medicine.

[27]  J. Taylor,et al.  FMS receptor for M-CSF (CSF-1) is sensitive to the kinase inhibitor imatinib and mutation of Asp-802 to Val confers resistance , 2006, Oncogene.

[28]  H. Kantarjian,et al.  Effects of AMN107, a novel aminopyrimidine tyrosine kinase inhibitor, on human mast cells bearing wild-type or mutated codon 816 c-kit. , 2005, Leukemia research.

[29]  J. Cornish,et al.  Deletion of Aspartate 182 in OPG Causes Juvenile Paget' Disease by Impairing Both Protein Secretion and Binding to RANKL , 2005, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[30]  J. Mestan,et al.  Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myeloid leukaemia. , 2005, Biochimica et biophysica acta.

[31]  F. Lordick,et al.  The systemic mastocytosis-specific activating cKit mutation D816V can be inhibited by the tyrosine kinase inhibitor AMN107 , 2005, Leukemia.

[32]  A. B. Lyons,et al.  Imatinib inhibits the functional capacity of cultured human monocytes , 2005, Immunology and cell biology.

[33]  Donna Neuberg,et al.  Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. , 2005, Cancer cell.

[34]  Ping Chen,et al.  Overriding Imatinib Resistance with a Novel ABL Kinase Inhibitor , 2004, Science.

[35]  J. Cornish,et al.  Mitogen-Activated Protein Kinase Signaling Pathways Subserve the Mitogenic and Antiapoptotic Actions of , 2022 .

[36]  A. B. Lyons,et al.  Imatinib inhibits the in vitro development of the monocyte/macrophage lineage from normal human bone marrow progenitors , 2003, Leukemia.

[37]  I. Reid,et al.  Lysophosphatidic Acid Is an Osteoblast Mitogen Whose Proliferative Actions Involve Gi Proteins and Protein Kinase C, But Not P42/44 Mitogen-Activated Protein Kinases. , 2001, Endocrinology.

[38]  I. Reid,et al.  Lysophosphatidic acid is an osteoblast mitogen whose proliferative actions involve G(i) proteins and protein kinase C, but not P42/44 mitogen-activated protein kinases. , 2001, Endocrinology.

[39]  I. Schieren,et al.  Mice deficient in Abl are osteoporotic and have defects in osteoblast maturation , 2000, Nature Genetics.

[40]  Sundeep Khosla,et al.  The Roles of Osteoprotegerin and Osteoprotegerin Ligand in the Paracrine Regulation of Bone Resorption , 2000, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[41]  I. Reid,et al.  Dissociation of the effects of amylin on osteoblast proliferation and bone resorption. , 1998, The American journal of physiology.

[42]  C. G. Groot,et al.  Osteocalcin antigenicity in cultured osteoblast-like cells after stimulation with 1,25-vitamin D3. , 1985, Cell biology international reports.

[43]  O. Bijvoet,et al.  A simple slide-rule method for the assessment of renal tubular reaborption of phosphate in man. , 1977, Clinica chimica acta; international journal of clinical chemistry.