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Treatment and management of myelofibrosis in the era of JAK inhibitors

Authors Keohane C, Radia DH, Harrison CN

Received 31 May 2013

Accepted for publication 16 July 2013

Published 20 August 2013 Volume 2013:7 Pages 189—198


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 4

Clodagh Keohane, Deepti H Radia, Claire N Harrison

Department of Haematology, Guy's and St Thomas' NHS Foundation Trust, London, UK

Abstract: Myelofibrosis (MF) can present as a primary disorder or evolve from polycythemia vera (PV) or essential thrombocythemia (ET) to post-PV MF or post-ET MF, respectively. MF is characterized by bone marrow fibrosis, splenomegaly, leukoerythroblastosis, extramedullary hematopoiesis, and a collection of debilitating symptoms. Until recently, the therapeutic options for patients with MF consisted of allogeneic hematopoietic stem cell transplant (alloHSCT), the use of cytoreductive agents (ie, hydroxyurea), splenectomy and splenic irradiation for treatment of splenomegaly, and management of anemia with transfusions, erythropoiesis-stimulating agents (ESAs), androgens, and immunomodulatory agents. However, with increased understanding of the pathogenesis of MF resulting from dysregulated Janus kinase (JAK) signaling, new targeted JAK inhibitor therapies, such as ruxolitinib, are now available. The purpose of this article is to review the clinical features of MF, discuss the use and future of JAK inhibitors, reassess when and how to use conventional MF treatments in the context of JAK inhibitors, and provide a perspective on the future of MF treatment.

Keywords: myelofibrosis, ruxolitinib, JAK inhibitor

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