Ugarte, Giorgia D.Vargas, Macarena F.Medina, Matías A.León, PabloNecuñir, DavidElorza, Alvaro A.Gutiérrez, Soraya E.Moon, Randall T.Loyola, AlejandraDe Ferrari, Giancarlo V.2023-03-062023-03-062015-100006-4971https://repositorio.unab.cl/xmlui/handle/ria/47344Indexación: ScopusChromosomal translocations are frequently associated with a wide variety of cancers, particularly hematologic malignancies. A recurrent chromosomal abnormality in acute myeloid leukemia is the reciprocal translocation t(8;21) that fuses RUNX1 and ETO genes. We report here that Wnt/β-catenin signaling increases the expression of ETO and RUNX1 genes in human hematopoietic progenitors. We found that β-catenin is rapidly recruited into RNA polymerase II transcription factories (RNAPII-Ser5) and that ETO and RUNX1 genes are brought into close spatial proximity upon Wnt3a induction. Notably, long-term treatment of cells with Wnt3a induces the generation a frequent RUNX1-ETO translocation event. Thus, Wnt/β-catenin signaling induces transcription and translocation of RUNX1 and ETO fusion gene partners, opening a novel window to understand the onset/development of leukemia. © 2015 by The American Society of Hematology.enMutationAcute Myeloid LeukemiaTranscription Factor RUNX1ArtículoAtribución 4.0 Internacional (CC BY 4.0)10.1182/blood-2015-04-638494