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Resident stem cells and renal carcinoma.

Bussolati B, Brossa A, Camussi G - Int J Nephrol (2011)

Bottom Line: 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.This suggests that renal cancer stem cells may contribute to the intratumor vasculogenesis.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Renal and Vascular Physiopathology, Department of Internal Medicine, Molecular Biotechnology Centre and Research Centre for Molecular Medicine, University of Turin, Cso Dogliotti 14, 10126 Turin, Italy.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Scheme representative of the possible stem cell origin of renal CSCs. Mutations/epigenetic alterations of the renal embryonic stem cells may originate the pediatric malignancy Wilm's tumor. The different histologic types of renal carcinomas of the adult may derive from mutations occurring in the stem cell compartment of the adult kidney. The lack of CD133+ marker in renal CSCs may support the idea of an origin from a yet unidentified mesenchymal population, which is ahead  of CD133+ renal progenitors in the differentiation linage. Alternatively, a process of de-differentiation of renal progenitors or mature cells could be involved.
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fig1: Scheme representative of the possible stem cell origin of renal CSCs. Mutations/epigenetic alterations of the renal embryonic stem cells may originate the pediatric malignancy Wilm's tumor. The different histologic types of renal carcinomas of the adult may derive from mutations occurring in the stem cell compartment of the adult kidney. The lack of CD133+ marker in renal CSCs may support the idea of an origin from a yet unidentified mesenchymal population, which is ahead of CD133+ renal progenitors in the differentiation linage. Alternatively, a process of de-differentiation of renal progenitors or mature cells could be involved.

Mentions: According to the hierarchical lineage view of tumors [20], renal tumors may arise from the embryonic stem cell compartment, giving rise to the Wilm's tumor, as well as from the stem cell pool of the adult kidney or from the deriving progenitors, giving rise to the different histologic types of carcinomas (undifferentiated, clear-cell, papillary carcinomas) (Figure 1). Embryonic stem cells have been described in the embryonic kidney until relatively late in gestation in the nephrogenic zone, from which they have been isolated and characterized [28]. Comparative analysis of embryonic stem cells and of the pediatric renal malignancy Wilm's tumor showed that Wilm's tumor resulted from a differentiation arrest of embryonic progenitors committed to the nephrogenic lineage [29]. These cells were present in the tumor both as undifferentiated blastema and as renal differentiated elements.


Resident stem cells and renal carcinoma.

Bussolati B, Brossa A, Camussi G - Int J Nephrol (2011)

Scheme representative of the possible stem cell origin of renal CSCs. Mutations/epigenetic alterations of the renal embryonic stem cells may originate the pediatric malignancy Wilm's tumor. The different histologic types of renal carcinomas of the adult may derive from mutations occurring in the stem cell compartment of the adult kidney. The lack of CD133+ marker in renal CSCs may support the idea of an origin from a yet unidentified mesenchymal population, which is ahead  of CD133+ renal progenitors in the differentiation linage. Alternatively, a process of de-differentiation of renal progenitors or mature cells could be involved.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3106374&req=5

fig1: Scheme representative of the possible stem cell origin of renal CSCs. Mutations/epigenetic alterations of the renal embryonic stem cells may originate the pediatric malignancy Wilm's tumor. The different histologic types of renal carcinomas of the adult may derive from mutations occurring in the stem cell compartment of the adult kidney. The lack of CD133+ marker in renal CSCs may support the idea of an origin from a yet unidentified mesenchymal population, which is ahead of CD133+ renal progenitors in the differentiation linage. Alternatively, a process of de-differentiation of renal progenitors or mature cells could be involved.
Mentions: According to the hierarchical lineage view of tumors [20], renal tumors may arise from the embryonic stem cell compartment, giving rise to the Wilm's tumor, as well as from the stem cell pool of the adult kidney or from the deriving progenitors, giving rise to the different histologic types of carcinomas (undifferentiated, clear-cell, papillary carcinomas) (Figure 1). Embryonic stem cells have been described in the embryonic kidney until relatively late in gestation in the nephrogenic zone, from which they have been isolated and characterized [28]. Comparative analysis of embryonic stem cells and of the pediatric renal malignancy Wilm's tumor showed that Wilm's tumor resulted from a differentiation arrest of embryonic progenitors committed to the nephrogenic lineage [29]. These cells were present in the tumor both as undifferentiated blastema and as renal differentiated elements.

Bottom Line: 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.This suggests that renal cancer stem cells may contribute to the intratumor vasculogenesis.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Renal and Vascular Physiopathology, Department of Internal Medicine, Molecular Biotechnology Centre and Research Centre for Molecular Medicine, University of Turin, Cso Dogliotti 14, 10126 Turin, Italy.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus