Myeloid cell differentiation arrest by miR-125b-1 in myelodysplasic syndrome and acute myeloid leukemia with the t(2;11)(p21;q23) translocation

Most chromosomal translocations in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) involve oncogenes that 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 tha...

Descripción completa

Detalles Bibliográficos
Autores principales: Bousquet, Marina, Quelen, Cathy, Rosati, Roberto, Mansat-De Mas, Véronique, La Starza, Roberta, Bastard, Christian, Lippert, Eric, Talmant, Pascaline, Lafage-Pochitaloff, Marina, Leroux, Dominique, Gervais, Carine, Viguié, Franck, Lai, Jean-Luc, Terre, Christine, Beverlo, Berna, Sambani, Costantina, Hagemeijer, Anne, Marynen, Peter, Delsol, Georges, Dastugue, Nicole, Mecucci, Cristina, Brousset, Pierre
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2008
Materias:
Brief Definitive Reports
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2571925/
https://www.ncbi.nlm.nih.gov/pubmed/18936236
http://dx.doi.org/10.1084/jem.20080285
Descripción
Sumario:Most chromosomal translocations in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) involve oncogenes that 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 associated with a strong up-regulation of miR-125b (from 6- to 90-fold). In vitro experiments revealed that miR-125b was able to interfere with primary human CD34(+) cell differentiation, and also inhibited terminal (monocytic and granulocytic) differentiation in HL60 and NB4 leukemic cell lines. 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 clinicopathological entity.

Ejemplares similares