Myeloid Cell Differentiation Arrest by Mir-125b-1 in Myelodysplasic Syndrome and Acute Myeloid Leukemia with the T(2;11)(p21;q23) Translocation

• Published in: Blood Vol. 112; no. 11; p. 4148
• Main Authors: Bousquet, Marina, Quelen, Cathy, Rosati, Roberto, Mas, Véronique Mansat-De, Bastard, Christian, Lippert, Eric, Talmant, Pascaline, Lafage-Pochitaloff, Marina, Leroux, Dominique, Gervais, Carine, Viguie, Franck, Lai, Jean-Luc, Terre, Christine, Delsol, Georges, Dastugue, Nicole, Mecucci, Cristina, Brousset, Pierre
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 16.11.2008
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.V112.11.4148.4148

Most chromosomal translocations in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) involve oncogenes which are either up-regulated or form part of new chimeric genes. The t(2;11)(p21;q23) translocation has been cloned in 19 cases of MDS and AML. In addition to this, we have shown that this translocation is responsible for a strong up-regulation of miR-125b (6 to 90 fold). In vitro experiments revealed that miR-125b was able to block monocytic and granulocytic differentiation of leukemic cells and primary CD34+ human blasts. Therefore, miR-125b up-regulation may represent a new mechanism of myeloid cell transformation and myeloid neoplasms carrying the t(2;11) translocation define a new clinico-pathological entity.