The Role of New Technologies in Myeloproliferative Neoplasms

Conclusions The discovery of JAK2V617F mutation in BCR-ABL1-negative MPNs by four different international cooperative groups in 2005 (2–5) led to significant insights on the pathogenesis of these disorders. In fact, this mutation results in a gain-of-function with activation of cytokine and growth factor receptors, and thus of the downstream JAK-STAT pathway (79, 95–98). The JAK2 point mutation in exon 12, present in a small percentage of patients with PV, is able to induce the MPN phenotype through the same pathogenic mechanism (6, 7). In 2006 the MPLW515L/K was reported in ET and PMF patients (44, 45) and demonstrated to be able to aberrantly activate JAK-STAT pathway through a gain-of function similar to that of JAK2, thus leading to megakaryocytic proliferation (8–10). More recently, in 2013 two different groups demonstrated a spectrum of mutations in CALR gene that cause frameshifts of one base pair in the last coding exon with a generation of a protein with new C terminus and a tail of 36 aminoacids (11, 12). Although it was soon clear that JAK-STAT signaling pathway was consistently activated in CALR mutated cells (53, 99), only recently it has been demonstrated that the mutant CALR protein is able to bind to the MPL receptor and activate it independently of the TPO presence itself (54–57). Consistently with the fact that all these mutations cause JAK-STAT pathway activation, ruxolitinib, the first JAK1/2 inhibitor, is able to exert clinical ...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research

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