JAK2V617F allele burden ⩾50% is associated with response to ruxolitinib in persons with MPN-associated myelofibrosis and splenomegaly requiring therapy

Correlation of mutation profile and response in patients with myelofibrosis treated with ruxolitinib

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Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis

(2014) R. Rampal et al.   BLOOD

Revised response criteria for myelofibrosis: International Working Group-Myeloproliferative Neoplasms Research and Treatment (IWG-MRT) and European LeukemiaNet (ELN) consensus report

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Identifying and addressing unmet clinical needs in Ph-neg classical myeloproliferative neoplasms: A consensus-based SIE, SIES, GITMO position paper

(2013) Giovanni Barosi et al.   LEUKEMIA RESEARCH

A Double-Blind, Placebo-Controlled Trial of Ruxolitinib for Myelofibrosis

(2012) Srdan Verstovsek et al.   NEW ENGLAND JOURNAL OF MEDICINE

JAK Inhibition with Ruxolitinib versus Best Available Therapy for Myelofibrosis

(2012) Claire Harrison et al.   NEW ENGLAND JOURNAL OF MEDICINE

A dynamic prognostic model to predict survival in primary myelofibrosis: a study by the IWG-MRT (International Working Group for Myeloproliferative Neoplasms Research and Treatment)

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Angiogenesis and vascular endothelial growth factor-/receptor expression in myeloproliferative neoplasms: correlation with clinical parameters andJAK2-V617Fmutational status

(2009) Michael Medinger et al.   BRITISH JOURNAL OF HAEMATOLOGY

JAK2 stimulates homologous recombination and genetic instability: potential implication in the heterogeneity of myeloproliferative disorders

(2008) I. Plo et al.   BLOOD