Different expression patterns of LGALS1 and LGALS3 in polycythemia vera, essential thrombocythemia and primary myelofibrosis

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Moura, L. G. ; Tognon, R. ; Nunes, N. S. ; Cataldi Rodrigues, L. ; Ferreira, A. F. ; Kashima, S. ; Covas, D. T. ; Santana, M. ; Souto, E. X. ; Perobelli, L. ; Simoes, B. P. ; Dias-Baruffi, M. ; Castro, F. A.

• Document type: Journal article
• Source: Journal of Clinical Pathology; v. 69, n. 10, p. 926-929, OCT 2016.
• Web of Science Citations: 2

Abstract

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. (AU)

• FAPESP's process: 10/11905-6 - Galectin-1 and 3 expression in chronic myeloproliferative diseases
• Grantee: Livia Gonzaga Moura
• Support Opportunities: Scholarships in Brazil - Master