A JAK2-V617F activating mutation in addition to KIT and FLT3 mutations is associated with clinical outcome in patients with t(8;21)(q22;q22) acute myeloid leukemia
暂无分享,去创建一个
H. Mitsuya | N. Matsuno | N. Asou | T. Nanri | T. Kawakita | Eisaku Iwanaga
[1] C. Pascutto,et al. Prognostic factors for thrombosis, myelofibrosis, and leukemia in essential thrombocythemia: a study of 605 patients , 2008, Haematologica.
[2] M. Odero,et al. JAK2-V617F activating mutation in acute myeloid leukemia: prognostic impact and association with other molecular markers , 2007, Leukemia.
[3] H. Mitsuya,et al. A JAK2-V617F Activating Mutation in Addition to C-KIT and FLT3 Mutations Is Associated with Clinical Outcome in Patients with t(8;21)(q22;q22;) Acute Myeloid Leukemia. , 2007 .
[4] C. Bloomfield,et al. Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: recommendations from an ad hoc international expert panel. , 2007, Blood.
[5] J. Ihle,et al. Jak2: normal function and role in hematopoietic disorders. , 2007, Current opinion in genetics & development.
[6] P. Lev,et al. JAK2V617F mutation in platelets from essential thrombocythemia patients: correlation with clinical features and analysis of STAT5 phosphorylation status , 2006, European journal of haematology.
[7] W. Hiddemann,et al. Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1‐ETO , 2006, British journal of haematology.
[8] F. Ferrara,et al. Prognostic impact of c-KIT mutations in core binding factor leukemias: an Italian retrospective study. , 2006, Blood.
[9] S. H. Lee,et al. The JAK2 V617F mutation in de novo acute myelogenous leukemias , 2006, Oncogene.
[10] K. Mitani,et al. A randomized, postremission comparison of four courses of standard‐dose consolidation therapy without maintenance therapy versus three courses of standard‐dose consolidation with maintenance therapy in adults with acute myeloid leukemia , 2005, Cancer.
[11] H. Mitsuya,et al. Mutations in the receptor tyrosine kinase pathway are associated with clinical outcome in patients with acute myeloblastic leukemia harboring t(8;21)(q22;q22) , 2005, Leukemia.
[12] N. Asou. The role of a Runt domain transcription factor AML1/RUNX1 in leukemogenesis and its clinical implications. , 2003, Critical reviews in oncology/hematology.
[13] N. Harris,et al. The World Health Organization (WHO) classification of the myeloid neoplasms. , 2002, Blood.
[14] T. Haferlach,et al. JAK2 seems to be a typical cooperating mutation in therapy-related t(8;21)/ AML1-ETO-positive AML , 2007, Leukemia.
[15] G. Ehninger,et al. Tyrosine kinase mutations of JAK2 are rare events in AML but influence prognosis of patients with CBF-leukemias. , 2007, Haematologica.
[16] K. Döhner,et al. JAK2V617F mutations as cooperative genetic lesions in t(8;21)-positive acute myeloid leukemia. , 2006, Haematologica.
[17] J. Laszlo,et al. Experience of the Polycythemia Vera Study Group with essential thrombocythemia: a final report on diagnostic criteria, survival, and leukemic transition by treatment. , 1997, Seminars in hematology.