Literature DB >> 12951584

The role of FLT3 in haematopoietic malignancies.

Derek L Stirewalt1, Jerald P Radich.   

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.

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Year:  2003        PMID: 12951584     DOI: 10.1038/nrc1169

Source DB:  PubMed          Journal:  Nat Rev Cancer        ISSN: 1474-175X            Impact factor:   60.716


  244 in total

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7.  Quizartinib-resistant FLT3-ITD acute myeloid leukemia cells are sensitive to the FLT3-Aurora kinase inhibitor CCT241736.

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Journal:  Blood Adv       Date:  2020-04-14

8.  Inhibition of the receptor tyrosine kinase Axl impedes activation of the FLT3 internal tandem duplication in human acute myeloid leukemia: implications for Axl as a potential therapeutic target.

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Journal:  Blood       Date:  2013-01-15       Impact factor: 22.113

9.  Development and Characterization of FLT3-Specific Curcumin-Loaded Polymeric Micelles as a Drug Delivery System for Treating FLT3-Overexpressing Leukemic Cells.

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10.  Meis1 programs transcription of FLT3 and cancer stem cell character, using a mechanism that requires interaction with Pbx and a novel function of the Meis1 C-terminus.

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