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At present, allo-SCT is the only curative treatment for patients with myelofibrosis (MF). Unfortunately, a significant proportion of candidate patients are considered transplant ineligible due to their poor general condition and advanced age at the time of diagnosis. The approval of the first JAK inhibitor, ruxolitinib, for patients with advanced MF in 2011 has had a qualified impact on the treatment algorithm. The drug affords substantial improvement in MF-associated symptoms and splenomegaly but no major effect on the natural history. There has, therefore, been considerable support for assessing the drug's candidacy in the peritransplant period. The drug's precise impact on clinical outcome following allo-SCT is currently not known; nor are the drug's long-term efficacy and safety known. Considering the rarity of MF and the small proportion of patients who undergo allo-SCT, well designed collaborative efforts are required. In order to address some of the principal challenges, an expert panel of laboratory and clinical experts in this field was established, and an independent workshop held during the 54th American Society of Hematology Annual Meeting in New Orleans, USA on 6 December 2013, and the European Hematology Association's Annual Meeting in Milan, Italy on 13 June 2014. This document summarizes the results of these efforts. [ABSTRACT FROM AUTHOR]

Ph-positive chronic myeloid leukemia (CML) and Ph-negative chronic myeloproliferative diseases (MPDs), characterized in many cases by the presence of the JAK2V617F mutation, have many features in common and yet also show fundamental differences. In this review, we pose five discrete and related questions relevant to both categories of hematological malignancy, namely: What are the mechanisms that underlie disease progression from a relatively benign or chronic phase? By what therapeutic methods might one target residual leukemia stem cells in CML? Is JAK2V617F the original molecular event in MPD? What epigenetic events must have a role in dictating disease phenotype in MPDs? And finally, Will the benefits conferred by current or future JAK2V617F inhibitors equal or even surpass the clinical success that has resulted from the use of tyrosine kinase inhibitors in CML? These and others questions must be addressed and in some cases should be answered in the foreseeable future. [ABSTRACT FROM AUTHOR]

The article discusses the common and different features of BCR-ABL1-positive chronic myeloid leukemia (CML) and BCR-ABL1-negative chronic myeloproliferative disorders. The BCR-ABL1-positive and the JAK2-positive MPNs provide important information on the earliest stages of tumorigenesis. Moreover, study of their molecular pathogenesis shows their differences in certain cases like determining molecular abnormalities. Meanwhile, tyrosine kinase inhibitors (TKIs) has been effective in CML treatment.

The article presents an editorial looking at chronic myeloid leukemia. The article discusses the part genomic instability plays in causing the BCR-ABL fusion, the PP2A tumor suppressor gene, resistance to imatinib mesylate, the possible association between imatinib mesylate and cardiac failure, the U.S. Food and Drug Administration's approval of dasatinib, and the therapeutic use of tyrosine kinase.