STAT3 mutations are frequent in CD30+ T-cell lymphomas and T-cell large granular lymphocytic leukemia

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R S Ohgami
L Ma
J D Merker
B Martinez
J L Zehnder
D A Arber
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[1] Stanford University Medical Center,
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Leukemia | 2013年 / 27卷
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页码:2244 / 2247
页数:3
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[1]  
Levy DE(2006)STAT3: a multifaceted oncogene Proc Natl Acad Sci USA 103 10151-10152
[2]  
Inghirami G(2007)Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome Nature 448 1058-1062
[3]  
Minegishi Y(2012)Somatic STAT3 mutations in large granular lymphocytic leukemia N Engl J Med 366 1905-1913
[4]  
Saito M(2012)STAT3 mutations unify the pathogenesis of chronic lymphoproliferative disorders of NK cells and T-cell large granular lymphocyte leukemia Blood 120 3048-3057
[5]  
Tsuchiya S(2003)Differential expression and clinical significance of tyrosine-phosphorylated STAT3 in ALK+ and ALK- anaplastic large cell lymphoma Clin Cancer Res 9 3692-3699
[6]  
Tsuge I(2001)Constitutive STAT3-activation in Sezary syndrome: tyrphostin AG490 inhibits STAT3-activation, interleukin-2 receptor expression and growth of leukemic Sezary cells Leukemia 15 787-793
[7]  
Takada H(2011)Refining the diagnosis of T-cell large granular lymphocytic leukemia by combining distinct patterns of antigen expression with T-cell clonality studies Leukemia 25 1439-1443
[8]  
Hara T(2005)Stat3 is required for ALK-mediated lymphomagenesis and provides a possible therapeutic target Nat Med 11 623-629
[9]  
Koskela HL(2005)Targeting Stat3 in cancer therapy Anticancer Drugs 16 601-607
[10]  
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