Biological properties of ligand-dependent activation of the MET receptor kinase in acute myeloid leukemia

[1]  Benjamin J. Raphael,et al.  Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia. , 2013, The New England journal of medicine.

[2]  E. Vellenga,et al.  A Proteomics and Transcriptomics Approach to Identify Leukemic Stem Cell (LSC) Markers* , 2012, Molecular & Cellular Proteomics.

[3]  Roman K. Thomas,et al.  Epidermal growth factor receptor (EGFR) signaling and covalent EGFR inhibition in lung cancer. , 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[4]  K. Coombes,et al.  Survivin is highly expressed in CD34(+)38(-) leukemic stem/progenitor cells and predicts poor clinical outcomes in AML. , 2012, Blood.

[5]  Jane Fridlyand,et al.  Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors , 2012, Nature.

[6]  Andrew L. Kung,et al.  Autocrine activation of the MET receptor tyrosine kinase in acute myeloid leukemia , 2012, Nature Medicine.

[7]  F. Ferrara.  New agents for acute myeloid leukemia: is it time for targeted therapies? , 2012, Expert opinion on investigational drugs.

[8]  Steven M Kornblau,et al.  Abnormal expression of FLI1 protein is an adverse prognostic factor in acute myeloid leukemia. , 2011, Blood.

[9]  K. Wilner,et al.  Pharmacokinetics (PK) of crizotinib (PF-02341066) in patients with advanced non-small cell lung cancer (NSCLC) and other solid tumors. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[10]  B. Druker,et al.  MET receptor sequence variants R970C and T992I lack transforming capacity. , 2010, Cancer research.

[11]  Dmitri I Svergun,et al.  Structural basis of hepatocyte growth factor/scatter factor and MET signalling. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[12]  L. Naldini,et al.  An uncleavable form of pro-scatter factor suppresses tumor growth and dissemination in mice. , 2004, The Journal of clinical investigation.

[13]  Christian Wiesmann,et al.  Crystal structure of the HGF β‐chain in complex with the Sema domain of the Met receptor , 2004, The EMBO journal.

[14]  D. Small,et al.  Lack of KIT or FMS internal tandem duplications but co-expression with ligands in AML. , 2004, Leukemia research.

[15]  David Eisenberg,et al.  Bioinformatic identification of potential autocrine signaling loops in cancers from gene expression profiles , 2001, Nature Genetics.

[16]  K. Bauer,et al.  Heparin induces dimerization and confers proliferative activity onto the hepatocyte growth factor antagonists NK1 and NK2 , 1996, The Journal of cell biology.

[17]  K. Zsebo,et al.  Effects of human stem cell factor (c-kit ligand) on proliferation of myeloid leukemia cells: heterogeneity in response and synergy with other hematopoietic growth factors. , 1992, Blood.

[18]  P. Pilch,et al.  Mechanism of epidermal growth factor receptor autophosphorylation and high-affinity binding. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[19]  M. Braun,et al.  Sequence of MET protooncogene cDNA has features characteristic of the tyrosine kinase family of growth-factor receptors. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[20]  M. Sporn,et al.  Autocrine secretion and malignant transformation of cells. , 1980, The New England journal of medicine.