English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/134239
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:


Loss of p53 exacerbates multiple myeloma phenotype by facilitating the reprogramming of hematopoietic stem/progenitor cells to malignant plasma cells by MafB

AuthorsVicente-Dueñas, Carolina ; González-Herrero, Inés ; García-Cenador, Begoña; García-Criado, Francisco Javier; Sánchez García, Isidro
KeywordsMouse models
Cancer stem cell
Cancer therapy
Cell reprogramming
Stem cells
Multiple myeloma
Issue Date2012
PublisherLandes Bioscience
CitationCell Cycle 11(20): 3896-3900 (2012)
AbstractMultiple myeloma (MM) is a serious, mostly incurable human cancer of malignant plasma cells. Chromosomal translocations afecting MAFB are present in a signifcant percentage of multiple myeloma patients. Genetically engineered Sca1-MafB mice, in which MafB expression is limited to hematopoietic stem/progenitor cells (HS/p-Cs), display the phenotypic features of MM. Contrary to many other types of cancer, it is not yet known if the p53 gene plays any essential role in the pathogenesis of this disease. Here, we show, taking advantage of the Sca1-MafB MM mouse model, that loss of p53 does not rescue the multiple myeloma disease, but instead accelerates its development and exacerbates the MM phenotype. therefore, the efciency of the MafB-induced MM reprogramming of normal HS/p-Cs to terminally diferentiated malignant plasma cells is enhanced by p53 defciency, in analogy to what happens in reprogramming to pluripotency. these results raise caution about interfering with p53 function when treating multiple myeloma.
Identifiersdoi: 10.4161/cc.22186
issn: 1538-4101
e-issn: 1551-4005
Appears in Collections:(IBMCC) Artículos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
Show full item record
Review this work

Related articles:

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