Journal
MOLECULAR CELL
Volume 6, Issue 3, Pages 693-704Publisher
CELL PRESS
DOI: 10.1016/S1097-2765(00)00067-8
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Funding
- NCI NIH HHS [P0I CA 66996] Funding Source: Medline
- NIDDK NIH HHS [P0I DK 50654] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA066996] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P01DK050654] Funding Source: NIH RePORTER
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STATE is activated in a broad spectrum of human hematologic malignancies. We addressed whether STATE 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.
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