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Evaluation of the Relationship between Janus Kinase 2 Mutational Burden and Clinical Findings in Adult Myeloproliferative Neoplasm Patients

Philadelphia-negative chronic myeloproliferative neoplasms (Ph-negative MPNs) consist mainly of polycythemia vera (PV), primary myelofibrosis (PMF) and essential thrombocythemia (ET) (1). Ph-negative MPNs are associated with various genetic abnormalities. One of these abnormalities is Janus kinase 2 (JAK2), a protein tyrosine kinase gene. It is associated with cellular growth and proliferation. The most common genetic mutation found in Ph-negative MPNs is the JAK2 V617F mutation, wherein phenylalanine replaces valine due to a point mutation in Codon 617. The JAK2 gene is located on the short arm of chromosome 9. This mutation increases tyrosine phosphorylation activity, resulting in hypersensitivity of hematopoietic progenitor cells to growth factors (2,3). Treatment options for MPN patients include acetylsalicylic acid (ASA), phlebotomy, and hydroxyurea. Where hydroxyurea cannot be used due to its side effects, interferon-alpha (IFN-α), JAK2 inhibitors (ruxolitinib) or busulfan are recommended (4). JAK2 inhibitors such as ruxolitinib are more effective for splenomegaly and clinical symptoms than clonal effects. Studies on target molecules except JAK2 are ongoing (5). The JAK2 V617F mutation occurs in approximately half of ET and PMF patients and in 90% of PV patients. Other common genetic abnormalities in MPNs include mutations in CALR and MPL. JAK2, CALR and MPL mutations have been listed under World Health Organization’s MPN diagnostic criteria (6). With the NGS (next-generation