FMS receptor for M-CSF (CSF-1) is sensitive to the kinase inhibitor imatinib and mutation of Asp-802 to Val confers resistance

[1]  A. B. Lyons,et al.  Macrophage colony-stimulating factor receptor c-fms is a novel target of imatinib. , 2005, Blood.

[2]  V. Perry The influence of systemic inflammation on inflammation in the brain: implications for chronic neurodegenerative disease , 2004, Brain, Behavior, and Immunity.

[3]  C. Mol,et al.  Switching on kinases: oncogenic activation of BRAF and the PDGFR family , 2004, Nature Reviews Cancer.

[4]  K. Wilson,et al.  Structural Basis for the Autoinhibition and STI-571 Inhibition of c-Kit Tyrosine Kinase* , 2004, Journal of Biological Chemistry.

[5]  S. Gabriel,et al.  EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy , 2004, Science.

[6]  Patricia L. Harris,et al.  Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. , 2004, The New England journal of medicine.

[7]  J. Pollard Tumour-educated macrophages promote tumour progression and metastasis , 2004, Nature Reviews Cancer.

[8]  N. Pryer,et al.  SU11248 inhibits tumor growth and CSF-1R-dependent osteolysis in an experimental breast cancer bone metastasis model , 2004, Clinical & Experimental Metastasis.

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

[10]  B. Druker,et al.  Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. , 2003, Blood.

[11]  H. Serve,et al.  A Single Amino Acid Exchange Inverts Susceptibility of Related Receptor Tyrosine Kinases for the ATP Site Inhibitor STI-571* 210 , 2003, The Journal of Biological Chemistry.

[12]  Olivier Hermine,et al.  Effect of tyrosine kinase inhibitor STI571 on the kinase activity of wild-type and various mutated c-kit receptors found in mast cell neoplasms , 2003, Oncogene.

[13]  G. Demetri,et al.  Management of malignant gastrointestinal stromal tumours. , 2002, The Lancet. Oncology.

[14]  P. Cohen Protein kinases — the major drug targets of the twenty-first century? , 2002, Nature reviews. Drug discovery.

[15]  Shan Zeng,et al.  The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors; kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations. , 2002, Blood.

[16]  J. Reilly Class III receptor tyrosine kinases: role in leukaemogenesis , 2002, British journal of haematology.

[17]  G. Mundy Directions of drug discovery in osteoporosis. , 2002, Annual review of medicine.

[18]  H. Aldskogius Regulation of microglia - potential new drug targets in the CNS , 2001, Expert opinion on therapeutic targets.

[19]  Y. Ma,et al.  Classes of c-KIT activating mutations: proposed mechanisms of action and implications for disease classification and therapy. , 2001, Leukemia research.

[20]  C. Sawyers,et al.  Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. , 2001, The New England journal of medicine.

[21]  Andrew V. Nguyen,et al.  Colony-Stimulating Factor 1 Promotes Progression of Mammary Tumors to Malignancy , 2001, The Journal of experimental medicine.

[22]  P. Seeburg,et al.  Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. , 2000, Science.

[23]  J. Melo,et al.  Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance. , 2000, Blood.

[24]  N. Dibb,et al.  Evidence that downregulation of the M-CSF receptor is not dependent upon receptor kinase activity , 1999, Oncogene.

[25]  W. Gullick,et al.  Cell specific transformation by c-fms activating loop mutations is attributable to constitutive receptor degradation , 1999, Oncogene.

[26]  J. Pollard Role of colony‐stimulating factor‐1 in reproduction and development , 1997, Molecular reproduction and development.

[27]  B. Kacinski CSF‐1 and its receptor in breast carcinomas and neoplasms of the female reproductive tract , 1997, Molecular Reproduction and Development.

[28]  Keith Glover,et al.  Progress in Applied Robust Control , 1995 .

[29]  P. Ralph,et al.  Expression of v-fms and c-fms in the hemopoietic cell line FDC-P1. , 1990, Growth factors.

[30]  L. Rohrschneider,et al.  Induction of macrophage colony-stimulating factor-dependent growth and differentiation after introduction of the murine c-fms gene into FDC-P1 cells , 1989, Molecular and cellular biology.

[31]  L. Rohrschneider,et al.  Activation of the feline c-fms proto-oncogene: Multiple alterations are required to generate a fully transformed phenotype , 1988, Cell.

[32]  J. Downing,et al.  A point mutation in the extracellular domain of the human CSF-1 receptor (c-fms proto-oncogene product) activates its transforming potential , 1988, Cell.

[33]  J. Ihle,et al.  The v-fms oncogene induces factor-independent growth and transformation of the interleukin-3-dependent myeloid cell line FDC-P1. , 1987, Molecular and cellular biology.

[34]  J. Pollard,et al.  Isolation and characterization of a cloned growth factor dependent macrophage cell line, BAC1.2F5 , 1987, Journal of cellular physiology.

[35]  M. Roussel,et al.  Transforming potential of the c-fms proto-oncogene (CSF-1 receptor) , 1987, Nature.

[36]  Charles J. Sherr,et al.  The c-fms proto-oncogene product is related to the receptor for the mononuclear phagocyte growth factor, CSF 1 , 1985, Cell.