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Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease.

Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease. Research Abstract Details 

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  • Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease. Abstract Text:

    b r baldwinB R Baldwin,l liL Li,k-f tseK-F Tse,s smallS Small,m collectorM Collector,k a whartenbyK A Whartenby,s j sharkisS J Sharkis,f rackeF Racke,d husoD Huso,d smallD Small,

    Evidence is continuing to accumulate that the FMS-like tyrosine kinase 3 (FLT3) receptor plays an important role in acute leukemias. Acute myeloid leukemia patients often express constitutive active mutant forms of the receptor in their leukemic cells. A t(12;13)(p13;q12) translocation between Tel and the FLT3 receptor was recently described in a patient with myeloproliferative disease (MPD). Here a Tel-FLT3 construct mimicking this fusion protein was used to generate transgenic mice. The fusion protein was previously found to constitutively activate FLT3 signaling and transform Ba/F3 cells. Expression of the fusion protein in the transgenic mice was found in all tissues assayed including spleen, bone marrow (BM), thymus and liver. These mice developed splenomegaly and had a high incidence of MPD with extramedullary hematopoiesis in the liver and lymph nodes. Spleens also had increased dendritic and natural killer cell populations. In vitro analysis of the hematopoietic progenitor cells derived from Tel-FLT3 transgenic mice showed a significant increase in the number of CFU-GM in the BM, and CFU-GM, BFU-E and CFU-GEMM in the spleen. BM also showed significant increases of in vivo CFU-S colonies. Thus, transgenic mice expressing constitutively activated Tel-FLT3 develop MPD with a long latency and also result in the expansion of the hematopoietic stem/progenitor cells.

    Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease. Publishing Authors By Initials

    br baldwinBR Baldwin,l liL Li,kf tseKF Tse,s smallS Small,m collectorM Collector,ka whartenbyKA Whartenby,sj sharkisSJ Sharkis,f rackeF Racke,d husoD Huso,d smallD Small,

    For similar enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-tyrosine kinases: receptor protein-tyrosine kinases: fms-like tyrosine kinase 3 research abstracts see: enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-tyrosine kinases: receptor protein-tyrosine kinases: fms-like tyrosine kinase 3 research

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    Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Leukemia : official journal of the Leukemia Societ

    VOLUME: 21

    Page Numbers: 764-71

    Journal Abbreviation: Leukemia

    ISSN: 0887-6924

    DAY: 1

    MONTH: 02

    YEAR: 2007

    Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8704895

    Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease. Keywords Mesh Terms:

    KEYWORDS: fms-Like Tyrosine Kinase 3

    MESH TERMS: genetics

    Chemical & Substance for Abstract: Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease. Information

    Substance Name: FLT3 protein, human

    Registry Number: EC 2.7.10.1

    Grant and Affiliation Information for Transgenic mice expressing Tel-FLT3, a constitutively activated form of FLT3, develop myeloproliferative disease.

    AFFILIATION: Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NCI

    GRANT: CA91177

    ACRONYM: CA

    MEDLINETA: Leukemia

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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