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Though it has been remarkable to have witnessed the major advances in the understanding of the molecular pathogenesis of the chronic myeloproliferative neoplasms (MPN) over the past three decades, many challenges remain. The advances began with the identification of the BCR-ABL1 gene in chronic myeloid leukemia (CML) in 1985, leading to the introduction of ABL1 tyrosine kinase inhibitors (TKIs), and the JAK2V617F mutation in polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) in 2005, leading to the JAK inhibitors.1–3 CML is now arguably the most successfully treated human malignancy. Despite these remarkable achievements, the quest for cure, functionally defined as treatment-free remission after discontinuation of TKI therapy, remains difficult.4 In the BCR-ABL1 negative MPNs, a similar degree of success has not been achieved, perhaps because of the rather surprising clonal complexity of these disorders and the increasing molecular evidence of the need for JAK2V617F mutation to cooperate with other genetic aberrations in the initiation and progression of the disease. This clonal complexity needs to be elucidated further in order to recognize clinically relevant candidate therapeutic targets. Herein, we review some of the topical challenges and successes in the biology and therapy of the MPNs that were discussed at the 7th post-American Society of Hematology CML-MPN workshop, which took place in Atlanta on December 11–12, 2012, and up-dated prior to this publication.

Current pre-clinical and clinical advances in the BCR-ABL1-positive and -negative chronic myeloproliferative neoplasms