| Literature DB >> 11030348 |
J Schwaller1, E Parganas, D Wang, D Cain, J C Aster, I R Williams, C K Lee, R Gerthner, T Kitamura, J Frantsve, E Anastasiadou, M L Loh, D E Levy, J N Ihle, D G Gilliland.
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.Entities:
Mesh：
Substances：
Year: 2000 PMID： 11030348 DOI： 10.1016/s1097-2765(00)00067-8
Source DB: PubMed Journal: Mol Cell ISSN： 1097-2765 Impact factor: 17.970