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Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2. Mol Cell 2000 Sep;6(3):693-704

Date

10/13/2000

Pubmed ID

11030348

DOI

10.1016/s1097-2765(00)00067-8

Scopus ID

2-s2.0-0033639119   256 Citations

Abstract

STAT5 is activated in a broad spectrum of human hematologic malignancies. We addressed whether STAT5 activation is necessary for the myelo- and lymphoproliferative disease induced by TEL/JAK2 using a genetic approach. Whereas mice transplanted with bone marrow transduced with retrovirus expressing TEL/JAK2 develop a rapidly fatal myelo- and lymphoproliferative syndrome, reconstitution with bone marrow derived from Stat5ab-deficient mice expressing TEL/JAK2 did not induce disease. Disease induction in the Stat5a/b-deficient background was rescued with a bicistronic retrovirus encoding TEL/JAK2 and Stat5a. Furthermore, myeloproliferative disease was induced by reconstitution with bone marrow cells expressing a constitutively active mutant, Stat5a, or a single Stat5a target, murine oncostatin M (mOSM). These data define a critical role for Stat5a/b and mOSM in the pathogenesis of TEL/JAK2 disease.

Author List

Schwaller J, Parganas E, Wang D, Cain D, Aster JC, Williams IR, Lee CK, Gerthner R, Kitamura T, Frantsve J, Anastasiadou E, Loh ML, Levy DE, Ihle JN, Gilliland DG

Author

Demin Wang PhD Assistant Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Blotting, Southern
Bone Marrow Cells
Bone Marrow Transplantation
Colony-Forming Units Assay
DNA, Neoplasm
DNA-Binding Proteins
Fibrosis
Flow Cytometry
Gene Transfer Techniques
Lymphoproliferative Disorders
Mice
Mice, Mutant Strains
Milk Proteins
Mutagenesis
Myeloproliferative Disorders
Neoplasm Transplantation
Oncogene Proteins, Fusion
Oncostatin M
Peptides
Phenotype
Retroviridae
STAT5 Transcription Factor
Trans-Activators
jenkins-FCD Prod-399 190a069c593fb5498b7fcd942f44b7bc9cdc7ea1