Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2

被引：258
|
作者：
Schwaller, J
Parganas, E
Wang, DM
Cain, D
Aster, JC
Williams, IR
Lee, CK
Gerthner, R
Kitamura, T
Frantsve, J
Anastasiadou, E
Loh, ML
Levy, DE
Ihle, JN
Gilliland, DG
机构：
[1] St Jude Childrens Res Hosp, Dept Biochem, Memphis, TN 38105 USA
[2] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Div Hematol & Oncol, Boston, MA 02115 USA
[4] Emory Univ, Dept Pathol, Atlanta, GA 30322 USA
[5] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA
[6] Univ Tokyo, Inst Med Sci, Tokyo 108, Japan
[7] Howard Hughes Med Inst, Coconut Grove, FL 33133 USA
来源：
MOLECULAR CELL | 2000年 / 6卷 / 03期
关键词：
D O I：
10.1016/S1097-2765(00)00067-8
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：693 / 704
页数：12
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