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of an activating mutation in JAK2 (the V617F mutation) as a STAT5 - activating and disease - causing genetic alteration in a significant proportion
of patients with myeloproliferative neoplasms (MPNs) has emphasized the oncogenic role
of the JAK tyrosine kinases in hematologic malignancies.2 — 5 JAK2 is a
member of the Janus tyrosine kinase
family comprising three other mammalian non-receptor tyrosine kinases (JAK1, JAK3 and TYK2) that associate with cytokine receptors lacking intrinsic kinase activity to mediate cytokine - induced signal transduction and activation
of STAT transcription factors.6 All JAKs share a similar protein structure and contain a tyrosine kinase domain at the C - terminus flanked by a catalytically inactive pseudokinase domain with kinase - regulatory activity, by an atypical SH2 domain and by a FERM domain that mediates association to the membrane - proximal region
of the cytokine receptors.7, 8 Soon
after the discovery
of JAK2 V617F, we and others described that activating JAK1 mutations are relatively common in adult patients with T - cell acute lymphoblastic leukemia (ALL) and participate in ALL development allowing for constitutive activation
of STAT5.9 — 11
Several STAT5 - activating JAK1 mutations were also reported in AML and breast cancer patients.10