Advances in the understanding of the pathogenesis of the myeloproliferative neoplasms (MPNs), polycythemia vera (PV) and primary myelofibrosis (MF), have led to improved treatment interventions. Approximately 95% of patients with PV and 50% of patients with MF have mutations in Janus kinase 2 (JAK2), which is essential for the normal development of granulocytes, erythrocytes, and platelets. Other less common shared mutations include CALR (calreticulin mutation) and MPL (myeloproliferative leukemia virus oncogene). Identification of mechanisms that cooperate with JAK-STAT signaling to predict disease progression and rationally guide the development of novel therapies is paramount to improving outcomes for patients.
June 5, 2022 | Hilton Chicago, IL
