TY - JOUR T1 - Different expression patterns of <em>LGALS1</em> and <em>LGALS3</em> in polycythemia vera, essential thrombocythemia and primary myelofibrosis JF - Journal of Clinical Pathology JO - J Clin Pathol SP - 926 LP - 929 DO - 10.1136/jclinpath-2016-203948 VL - 69 IS - 10 AU - L G Moura AU - R Tognon AU - N S Nunes AU - L Cataldi Rodrigues AU - A F Ferreira AU - S Kashima AU - D T Covas AU - M Santana AU - E X Souto AU - L Perobelli AU - B P Simões AU - M Dias-Baruffi AU - F A Castro Y1 - 2016/10/01 UR - http://jcp.bmj.com/content/69/10/926.abstract N2 - Despite all the knowledge, the cellular and molecular mechanisms involved in myeloproliferative neoplasm (MPN) pathophysiology remain unclear. Authors have shown galectin-1 (Gal-1) and 3 playing roles in tumour angiogenesis and fibrosis, which were correlated with poor prognosis in patients with MPN. In the present study LGALS1 and LGALS3 were differently expressed between polycythemia vera, essential thrombocythemia (ET) and primary myelofibrosis (PMF) diseases. Increased LGALS3 expression was associated with a negative JAK2 V617F status mutation in leucocytes from PMF but not in patients with ET without this mutation. However, a positive Janus kinase 2 (JAK2) V617F cell line established from patients with ET (SET-2 cells) when treated with JAK inhibitor presented high levels of LGALS3. Additionally, high LGALS1 expression was found in CD34+ cells but not in leucocytes from patients with PMF, in absence of JAK2 V617F mutation, and also in SET-2 cells treated with JAK inhibitor. Thus, our findings indicate that differential expression of LGALS1 and/or LGALS3 in patients with MPN is linked with JAK2 V617F status mutation in these diseases and state of cell differentiation. ER -