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Resident Stem Cells and Renal Carcinoma

According to the cancer stem cell hypothesis tumors are maintained by a cancer stem cell population which is able to initiate and maintain tumors. Tumor-initiating stem cells display stem or progenitor cell properties such as self-renewal and capacity to re-establish tumors that recapitulate the tum...

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Detalles Bibliográficos
Autores principales: Bussolati, Benedetta, Brossa, Alessia, Camussi, Giovanni
Formato: Texto
Lenguaje:English
Publicado: SAGE-Hindawi Access to Research 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106374/
https://www.ncbi.nlm.nih.gov/pubmed/21647312
http://dx.doi.org/10.4061/2011/286985
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author Bussolati, Benedetta
Brossa, Alessia
Camussi, Giovanni
author_facet Bussolati, Benedetta
Brossa, Alessia
Camussi, Giovanni
author_sort Bussolati, Benedetta
collection PubMed
description According to the cancer stem cell hypothesis tumors are maintained by a cancer stem cell population which is able to initiate and maintain tumors. Tumor-initiating stem cells display stem or progenitor cell properties such as self-renewal and capacity to re-establish tumors that recapitulate the tumor of origin. In this paper, we discuss data relative to the presence of cancer stem cells in human renal carcinoma and their possible origin from normal resident stem cells. The cancer stem cells identified in human renal carcinomas are not derived from the normal CD133(+) progenitors of the kidney, but rather from a more undifferentiated population that retains a mesenchymal phenotype. This population is able to self-renewal, clonogenicity, and in vivo tumor initiation. Moreover, they retain pluripotent differentiation capability, as they can generate not only the epithelial component of the tumor, but also tumor endothelial cells. This suggests that renal cancer stem cells may contribute to the intratumor vasculogenesis.
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spelling pubmed-31063742011-06-06 Resident Stem Cells and Renal Carcinoma Bussolati, Benedetta Brossa, Alessia Camussi, Giovanni Int J Nephrol Review Article According to the cancer stem cell hypothesis tumors are maintained by a cancer stem cell population which is able to initiate and maintain tumors. Tumor-initiating stem cells display stem or progenitor cell properties such as self-renewal and capacity to re-establish tumors that recapitulate the tumor of origin. In this paper, we discuss data relative to the presence of cancer stem cells in human renal carcinoma and their possible origin from normal resident stem cells. The cancer stem cells identified in human renal carcinomas are not derived from the normal CD133(+) progenitors of the kidney, but rather from a more undifferentiated population that retains a mesenchymal phenotype. This population is able to self-renewal, clonogenicity, and in vivo tumor initiation. Moreover, they retain pluripotent differentiation capability, as they can generate not only the epithelial component of the tumor, but also tumor endothelial cells. This suggests that renal cancer stem cells may contribute to the intratumor vasculogenesis. SAGE-Hindawi Access to Research 2011-05-11 /pmc/articles/PMC3106374/ /pubmed/21647312 http://dx.doi.org/10.4061/2011/286985 Text en Copyright © 2011 Benedetta Bussolati et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Bussolati, Benedetta
Brossa, Alessia
Camussi, Giovanni
Resident Stem Cells and Renal Carcinoma
title Resident Stem Cells and Renal Carcinoma
title_full Resident Stem Cells and Renal Carcinoma
title_fullStr Resident Stem Cells and Renal Carcinoma
title_full_unstemmed Resident Stem Cells and Renal Carcinoma
title_short Resident Stem Cells and Renal Carcinoma
title_sort resident stem cells and renal carcinoma
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106374/
https://www.ncbi.nlm.nih.gov/pubmed/21647312
http://dx.doi.org/10.4061/2011/286985
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