Role of Additional Novel Therapies in Myeloproliferative Neoplasms

被引：3
|
作者：
Fiskus, Warren [1 ]
Ganguly, Siddhartha [2 ]
Kambhampati, Suman [2 ]
Bhalla, Kapil N. [1 ]
机构：
[1] Univ Kansas, Med Ctr, Kansas City, KS 66160 USA
[2] Univ Kansas, Dept Hematol Oncol, Med Ctr, Westwood, KS 66205 USA
来源：
HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA | 2012年 / 26卷 / 05期
关键词：
JAK2-V617F; HDAC inhibitor; hsp90; inhibitors; PI3K/AKT inhibitor; MEK inhibitor; Myeloproliferative neoplasms; HISTONE DEACETYLASE INHIBITORS; CHRONIC MYELOMONOCYTIC LEUKEMIA; CHROMATIN-MODIFYING AGENTS; ACUTE MYELOGENOUS LEUKEMIA; STEM-CELL TRANSPLANTATION; TYROSINE KINASE JAK2; PROTEIN; 90; INHIBITOR; POLYCYTHEMIA-VERA; ONCOMETABOLITE; 2-HYDROXYGLUTARATE; ESSENTIAL THROMBOCYTHEMIA;
D O I：
10.1016/j.hoc.2012.07.001
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
The recent approval of ruxolitinib (INCB018424) for myelofibrosis and the preclinical/clinical development of several additional Janus kinase (JAK)targeted agents have ushered in an era of novel therapies for advanced myeloproliferative neoplasms (MPN), which are associated with constitutive activation of the JAK signal transducer and activation of transcription (STAT) signaling pathway. Collectively, these novel therapeutic approaches could rapidly broaden the spectrum of available therapies, with potential for improved clinical outcome for patients with advanced MPN. This review covers the recent developments in the testing of novel therapeutic agents other than JAK inhibitors that target signaling pathways in addition to JAK/STAT, or target the deregulated epigenetic mechanisms in MPN.
引用
收藏
页码：959 / +
页数：23
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