English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/173858
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:


Glioblastoma Bystander Cell Therapy: Improvements in Treatment and Insights into the Therapy Mechanisms

AuthorsGuerra-Rebollo, Marta; Nogueira De Moraes, Carolina; Alcoholado, Cristina; Soler-Botija, Carolina; Sánchez-Cid, Lourdes; Vila, Olaia F.; Meca-Cortés, Óscar ; Ramos-Romero, Sara; Rubio, Núria ; Becerra, J.; Blanco, Jerónimo ; Garrido, Cristina
KeywordsMesenchymal Stromal Cells
Issue Date21-Dec-2018
CitationMolecular Therapy - Oncolytics 11: 39-51 (2018)
AbstractA preclinical model of glioblastoma (GB) bystander cell therapy using human adipose mesenchymal stromal cells (hAMSCs) is used to address the issues of cell availability, quality, and feasibility of tumor cure. We show that a fast proliferating variety of hAMSCs expressing thymidine kinase (TK) has therapeutic capacity equivalent to that of TK-expressing hAMSCs and can be used in a multiple-inoculation procedure to reduce GB tumors to a chronically inhibited state. We also show that up to 25% of unmodified hAMSCs can be tolerated in the therapeutic procedure without reducing efficacy. Moreover, mimicking a clinical situation, tumor debulking previous to cell therapy inhibits GB tumor growth. To understand these striking results at a cellular level, we used a bioluminescence imaging strategy and showed that tumor-implanted therapeutic cells do not proliferate, are unaffected by GCV, and spontaneously decrease to a stable level. Moreover, using the CLARITY procedure for tridimensional visualization of fluorescent cells in transparent brains, we find therapeutic cells forming vascular-like structures that often associate with tumor cells. In vitro experiments show that therapeutic cells exposed to GCV produce cytotoxic extracellular vesicles and suggest that a similar mechanism may be responsible for the in vivo therapeutic effectiveness of TK-expressing hAMSCs. © 2018 The Author(s)
Appears in Collections:(IQAC) Artículos
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.