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Keohane C, Radia DH, Harrison CN. Biologics: Targets and Therapy. 2013;7:189–198. On page 193 note that the paragraph beginning "Pacritinib (SB1518; Cell Technology, Inc, Mountain View, CA, USA) is a JAK2 and FLT3 inhibitor currently being evaluated at a dose of 400 mg daily in a Phase II study (N=34) that included patients with low platelet counts (<50 × 109/L)." should have been "Pacritinib (SB1518; Cell Therapeutics, Inc, Seattle, WA, USA) is a JAK2 and FLT3 inhibitor which was evaluated at a dose of 400 mg daily in a Phase II study (N=34) that included patients with low platelet counts (<50 × 109/L)." On page 193 in the same paragraph note that "Post-Essential Thrombocythemia Myelofibrosis: PERSIST)." should have been "Post-Essential Thrombocythemia Myelofibrosis-1: PERSIST-1)."Read the original article

Clodagh Keohane, Deepti H Radia, Claire N HarrisonDepartment of Haematology, Guy's and St Thomas' NHS Foundation Trust, London, UKAbstract: 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 inhibitorCorrigendum for this article has been published