ABSTRACT
Polycythemia vera (PV) is a myeloproliferative neoplasm (MPN) characterized by increased and autonomous production of red cells and to lesser degree, other myeloid cells [1–9]. The abnormal proliferation in PV is caused by a constitutively active Janus kinase and signal transduction and activator of transcription (JAK-STAT) signal transduction pathway, due to unique V617F mutation within exon 14 (∼95% of PV) [10–12] and by different mutation within exon 12 (∼4% of PV) of the JAK2 gene [13,14].
