Abstract
Normal haematopoietic cells use complex systems to control proliferation, differentiation and cell death. The control of proliferation is, in part, accomplished through the ligand-induced stimulation of receptor tyrosine kinases, which signal to downstream effectors through the RAS pathway. Recently, mutations in the FMS-like tyrosine kinase 3 (FLT3) gene, which encodes a receptor tyrosine kinase, have been found to be the most common genetic lesion in acute myeloid leukaemia (AML), occurring in approximately 25% of cases. Exploring the mechanism by which these FLT3 mutations cause uncontrolled proliferation might lead to a better understanding of how cells become cancerous and provide insights for the development of new drugs.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Acute Disease
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Cell Division / genetics
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Cell Division / immunology
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / immunology
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Hematologic Neoplasms / genetics*
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Hematologic Neoplasms / immunology
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Humans
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Immune System / immunology
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Leukemia, Myeloid / genetics
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Leukemia, Myeloid / immunology
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Ligands
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Membrane Proteins / biosynthesis
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Membrane Proteins / genetics*
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Membrane Proteins / immunology
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Mutation / genetics
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Proto-Oncogene Proteins / biosynthesis
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Proto-Oncogene Proteins / genetics*
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Proto-Oncogene Proteins / immunology
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Receptor Protein-Tyrosine Kinases / biosynthesis
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Receptor Protein-Tyrosine Kinases / genetics*
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Receptor Protein-Tyrosine Kinases / immunology
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Receptors, Cell Surface / genetics*
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Receptors, Cell Surface / immunology
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Signal Transduction / genetics
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Signal Transduction / immunology
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fms-Like Tyrosine Kinase 3
Substances
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Ligands
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Membrane Proteins
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Proto-Oncogene Proteins
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Receptors, Cell Surface
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flt3 ligand protein
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FLT3 protein, human
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Receptor Protein-Tyrosine Kinases
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fms-Like Tyrosine Kinase 3