Abstract

Myeloproliferative neoplasms (MPN) arise from hematopoietic stem cells with somatically altered tyrosine kinase signaling. The World Health Organization (WHO) classifies them according to the presence of the BCR/ABL translocation in BCR/ABL positive chronic myelogenous leukemia (CML) and those which do not express BCR/ABL including; polycythemia vera, essential thrombocytosis and primary myelofibrosis. This last group is characterized by the expression of other mutations such as JAK2, MPL and CALR. JAK2, the most common, occurs in approximately 50% of cases (1, 2). According to literature, BCR/ABL and JAK2 are mutually exclusive (1, 2), however in some cases they can coexist. Two hypotheses have been postulated. The first one proposes that exists two cell clones, exhibiting each one, one mutation. Under treatment pressure of the dominant clone, the other one becomes over expressed. The second hypothesis states that exists one cell clone that simultaneously expresses both mutations (3, 4).

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