Prospect of JAK2 inhibitor therapy in myeloproliferative neoplasms

被引:5
作者
Atallah, Ehab [2 ]
Verstovsek, Srdan [1 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Leukemia Dept, Houston, TX 77030 USA
[2] Med Coll Wisconsin, Milwaukee, WI 53226 USA
关键词
essential thrombocythemia; JAK2; inhibitor; myelofibrosis; myeloproliferative neoplasm; polycythemia vera; TYROSINE KINASE JAK2; CONSTITUTIVE ACTIVATION; POLYCYTHEMIA-VERA; MULTIPLE-MYELOMA; MUTATION; PROLIFERATION; MYELOFIBROSIS; LEUKEMIA; PHOSPHORYLATION; APOPTOSIS;
D O I
10.1586/ERA.09.14
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The discovery of the Janus kinase (JAK)2 V617F mutation in patients with myeloproliferative neoplasms was a major milestone in understanding the biology of those disorders. Several groups simultaneously reported on the high incidence of this mutation in patients with myeloproliferative neoplasms: almost all patients with polycythemia vera harbor the mutation and about 50% of patients with essential thrombocythemia and primary myelofibrosis have the mutation, making the development of JAK2 tyrosine kinase inhibitors an attractive therapeutic goal. In addition, inhibition of JAK2 kinase may have a therapeutic role in other hematologic malignancies, such as chronic myeloid leukemia or lymphoma. A number of molecules that inhibit JAK2 kinase have been described in the literature, and several are being evaluated in a clinical setting. Here, we summarize current clinical experience with JAK2 inhibitors.
引用
收藏
页码:663 / 670
页数:8
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