English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/134207
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

Title

Essential role for telomerase in chronic myeloid leukemia induced by BCR-ABL in mice

AuthorsVicente-Dueñas, Carolina ; Barajas-Diego, Marcos ; Romero-Camarero, Isabel ; González-Herrero, Inés ; Flores, Teresa; Sánchez García, Isidro
Issue Date2012
PublisherImpact Journals
CitationOncotarget 3(3): 261-266 (2012)
AbstractThe telomerase protein is constitutively activated in malignant cells from many patients with cancer, including the chronic myeloid leukemia (CML), but whether telomerase is essential for the pathogenesis of this disease is not known. Here, we used telomerase deficient mice to determine the requirement for telomerase in CML induced by BCR-ABL in mouse models of CML. Loss of one telomerase allele or complete deletion of telomerase prevented the development of leukemia induced by BCR-ABL. However, BCR-ABL was expressed and active in telomerase heterozygous and null leukemic hematopoietic stem cells. These results demonstrate that telomerase is essential for oncogene-induced reprogramming of hematopoietic stem cells in CML development and validate telomerase and the genes it regulates as targets for therapy in CML.
DescriptionThis work is licensed under a Creative Commons Attribution 3.0 License.
Publisher version (URL)http://dx.doi.org/10.18632/oncotarget.461
URIhttp://hdl.handle.net/10261/134207
DOI10.18632/oncotarget.461
Identifiersdoi: 10.18632/oncotarget.461
e-issn: 1949-2553
Appears in Collections:(IBMCC) Artículos
Files in This Item:
File Description SizeFormat 
BCR-ABLinmice.pdf3,28 MBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.