Dear Colleagues,

The myeloproliferative neoplasms (MPN) are a group of rare chronic disorders characterized by the clonal proliferation of one or more blood cell lines in the myeloid lineage, and include primary myelofibrosis (PMF), chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia not otherwise specified (CEL-NOS), and MPN unclassifiable (MPN-U).

As a result of increasingly economical and available next-generation sequencing technologies, genetic studies in the past decade have improved our understanding of the molecular basis of MPNs. Recent breakthroughs include the discovery of activating mutations in CSF3R in the majority of patients with CNL, the presence of a driver mutation in the JAK2, MPL or CALR genes in ET and PMF (and the JAK2V617F mutation in approximately 95% of patients with PV), as well as activating mutations of KIT in some patients with CEL-NOS. Also, some very rare cases of familial hereditary MPNs have been described, caused by inherted germline mutations.

MPNs often progress to fibrosis or acute leukemia, both associated with very poor clinical outcome. Besides defining biomarkers for diagnosis, mutational studies have revealed the prognostic relevance of many somatic mutations, helping to improve the risk stratification of patients with MPNs.

Finally, knowledge of the molecular basis of MPNs has helped identify targets for directed therapy. The constitutive activation of tyrosine kinases in hematopoietic stem cells is a common molecular basis of the MPNs, with tyrosine kinase inhibitor therapy (such as imatinib, dasatinib, ruxolitinib or midostaurin) used with varying degrees of success to treat MPN. Other molecular mechanisms have also been revealed and numerous agents in various stages of development as single or combination therapies. Despite such advancements, our understanding of the molecular pathogenesis of the MPNs – particularly CNL, CEL-NOS and MPN-U – is still insufficient and treatment options limited.

In this Special Issue we are particularly interested in original papers and review articles that address developments in our understanding of the molecular basis of myelofibrosis and the MPNs, as well as manuscripts related to the keywords listed below.

Dr. María Teresa Gómez-Casares
Dr. Ruth Stuckey
Guest Editors

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• Molecular mechanisms of disease
• Next-generation sequencing
• Molecular screening
• Transformation to acute leukemia
• Genetically-improved prognostic models
• Fibrotic progression to fibrosis
• Prediction of thrombotic risk
• Germline predisposition
• Novel targeted therapies