Methylated Alteration of SHP1 and Mutation of JAK2 Tyrosine Kinase in Myeloproliferative Neoplasms

Philadelphia-negative myeloproliferative neoplasms (MPNs), mainly including polycythaemia vera (PV), essential thrombocythaemia (ET) and idiopathic myelofibrosis (IMF), represent a wide range of clonal hematological stem cell malignancies(Tefferi and Vardiman, 2008). Constitutive activation of Janus kinase 2/signal transducers and activators of transcription (JAK2/STAT) signaling caused by JAK2V617F mutation is considered to be the major pathogenesis of MPNs (James et al., 2005; Levine et al., 2005). The JAK2V617F mutation in Exon 14 has been observed in almost 98% of patients with PV and 50-60% of patients with ET and IMF. Other mutations such as JAK2 mutation in Exon 12(Pietra et al., 2008), thrombopoietin receptor (MPL515) mutation (Pardanani et al., 2006) and mutation in the inhibitory adaptor protein LNK (Oh et al., 2010) also