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http://dspace.hmtu.edu.vn/handle/DHKTYTHD_123/381
Nhan đề : | JAK inhibition in the myeloproliferative neoplasms: lessons learned from the bench and bedside |
Tác giả : | Gotlib, Jason |
Năm xuất bản : | 2013 |
Nhà xuất bản : | American Society of Hematology |
Tóm tắt : | The discovery of the JAK2 V617F mutation in the classic BCR-ABL1–negative myeloproliferative neoplasms in 2005 catalyzed a burst of research efforts that have culminated in substantial dividends for patients. Beyond JAK2 V617F, a more detailed picture of the pathobiologic basis for activated JAK-STAT signaling has emerged. In some patients with myelofibrosis (MF), next-generation sequencing technologies have revealed a complex clonal architecture affecting both genetic and epigenetic regulators of cell growth and differentiation. Although these bench-top findings have informed the clinical development of JAK inhibitors in MF, they have also provided scientific context for some of their limitations. The JAK1/JAK2 inhibitor ruxolitinib is approved for treatment of MF in North America and Europe and other lead JAK inhibitors discussed herein (fedratinib [SAR302503], momelotinib [CYT387], and pacritinib [SB1518]), have entered advanced phases of trial investigation. Uniformly, these agents share the ability to reduce spleen size and symptom burden. A major challenge for practitioners is how to optimize dosing of these agents to secure clinically relevant and durable benefits while minimizing myelosuppression. Suboptimal responses have spurred a “return to the bench” to characterize the basis for disease persistence and to inform new avenues of drug therapy. |
URI: | http://220.231.117.85:8000/handle/DHKTYTHD_123/381 |
Bộ sưu tập | Huyết học = Hematology |
Danh sách tệp tin đính kèm:
Tên tệp tin | Mô tả tệp tin | Dung lượng | Định dạng | |
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Hematology-2013-Gotlib-529-37.pdf Restricted Access | 1.98 MB | Adobe PDF | Gửi yêu cầu |
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