Summary
Abstract Introduction: Myeloproliferative neoplasms (MPN) are associated with both a higher risk of thrombosis and bleeding. Interestingly, both hyper- and hypo-reactivity in platelets is characteristic for MPN patients, the latter being the result of cellular exhaustion. The majority (>90%) of MPN have activating mutations in JAK2, a kinase operating downstream of the platelet/megakaryocyte receptor for thrombopoietin (TPO), c-Mpl. JAK2 mutations or TPO binding to c-Mpl lead to intracellular signaling in platelets, including phosphoinositide-3-kinase (PI3K). However, TPO is a platelet “primer”, i.e. it does not cause platelet aggregation itself, but synergizes with other agonists in converting the main platelet integrin, αIIbβ3, from a bent, low affinity (B+) to an extended, high a
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