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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004387naa a2200469 4500
001oai:DiVA.org:uu-203289
003SwePub
008130708s2013 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2032892 URI
0247 a https://doi.org/10.1186/1741-7015-11-1392 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Belmar-Lopez, Carolina4 aut
2451 0a Tissue-derived mesenchymal stromal cells used as vehicles for anti-tumor therapy exert different in vivo effects on migration capacity and tumor growth
264 c 2013-05-28
264 1b Springer Science and Business Media LLC,c 2013
338 a electronic2 rdacarrier
520 a Background: Mesenchymal stem cells (MSCs) have been promoted as an attractive option to use as cellular delivery vehicles to carry anti-tumor agents, owing to their ability to home into tumor sites and secrete cytokines. Multiple isolated populations have been described as MSCs, but despite extensive in vitro characterization, little is known about their in vivo behavior. The aim of this study was to investigate the efficacy and efficiency of different MSC lineages derived from five different sources (bone marrow, adipose tissue, epithelial endometrium, stroma endometrium, and amniotic membrane), in order to assess their adequacy for cell-based anti-tumor therapies. Our study shows the crucial importance of understanding the interaction between MSCs and tumor cells, and provides both information and a methodological approach, which could be used to develop safer and more accurate targeted therapeutic applications. Methods: We first measured the in vivo migration capacity and effect on tumor growth of the different MSCs using two imaging techniques: (i) single-photon emission computed tomography combined with computed tomography (SPECT-CT), using the human sodium iodine symporter gene (hNIS) and (ii) magnetic resonance imaging using superparamagnetic iron oxide. We then sought correlations between these parameters and expression of pluripotency-related or migration-related genes. Results: Our results show that migration of human bone marrow-derived MSCs was significantly reduced and slower than that obtained with the other MSCs assayed and also with human induced pluripotent stem cells (hiPSCs). The qPCR data clearly show that MSCs and hiPSCs exert a very different pluripotency pattern, which correlates with the differences observed in their engraftment capacity and with their effects on tumor growth. Conclusion: This study reveals differences in MSC recruitment/migration toward the tumor site and the corresponding effects on tumor growth. Three observations stand out: 1) tracking of the stem cell is essential to check the safety and efficacy of cell therapies; 2) the MSC lineage to be used in the cell therapy needs to be carefully chosen to balance efficacy and safety for a particular tumor type; and 3) different pluripotency and mobility patterns can be linked to the engraftment capacity of the MSCs, and should be checked as part of the clinical characterization of the lineage.
653 a Mesenchymal stromal cells
653 a Migration
653 a In vivo imaging
653 a Tumor growth
653 a Pluripotency
7001 a Mendoza, Gracia4 aut
7001 a Öberg, Danielu Uppsala universitet,Institutionen för medicinsk biokemi och mikrobiologi4 aut0 (Swepub:uu)daobe475
7001 a Burnet, Jerome4 aut
7001 a Simon, Carlos4 aut
7001 a Cervello, Irene4 aut
7001 a Iglesias, Maite4 aut
7001 a Carlos Ramirez, Juan4 aut
7001 a Lopez-Larrubia, Pilar4 aut
7001 a Quintanilla, Miguel4 aut
7001 a Martin-Duque, Pilar4 aut
7102 a Uppsala universitetb Institutionen för medicinsk biokemi och mikrobiologi4 org
7730 t BMC Medicined : Springer Science and Business Media LLCg 11, s. 139-q 11<139-x 1741-7015
8564 u https://uu.diva-portal.org/smash/get/diva2:636192/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 u https://bmcmedicine.biomedcentral.com/track/pdf/10.1186/1741-7015-11-139
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-203289
8564 8u https://doi.org/10.1186/1741-7015-11-139

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