| Literature DB >> 25597017 |
Laura S Danielson1, Linsey Reavie1, Marc Coussens1, Veronica Davalos1, Mireia Castillo-Martin2, Maria V Guijarro1, Maryaline Coffre1, Carlos Cordon-Cardo2, Iannis Aifantis1, Sherif Ibrahim1, Cynthia Liu1, Sergei B Koralov3, Eva Hernando4.
Abstract
The overexpression of microRNA cluster miR-17-92 has been implicated in development of solid tumors and hematological malignancies. The role of miR-17-92 in lymphomagenesis has been extensively investigated; however, because of the developmental defects caused by miR-17-92 dysregulation, its ability to drive tumorigenesis has remained undetermined until recently. Here we demonstrate that overexpression of miR-17-92 in a limited number of hematopoietic cells is sufficient to cause B cell malignancies. In sum, our study provides a novel and physiologically relevant model that exposes the potent ability of miR-17-92 to act as a driver of tumorigenesis.Entities:
Keywords: Lymphoma; Mouse model; miR-17-92
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Year: 2014 PMID： 25597017 PMCID： PMC4376677 DOI： 10.1016/j.leukres.2014.12.002
Source DB: PubMed Journal: Leuk Res ISSN： 0145-2126 Impact factor: 3.156