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Cancer Stem Cells and Pediatric Solid Tumors.

Friedman GK, Gillespie GY - Cancers (Basel) (2011)

Bottom Line: Recently, a subpopulation of cells, termed tumor-initiating cells or tumor stem cells (TSC), has been identified in many different types of solid tumors.Much of the research on TSC has focused on adult cancers.With considerable differences in tumor biology between adult and pediatric cancers, there may be significant differences in the presence, function and behavior of TSC in pediatric malignancies.

View Article: PubMed Central - PubMed

Affiliation: Division of Pediatric Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.

ABSTRACT
Recently, a subpopulation of cells, termed tumor-initiating cells or tumor stem cells (TSC), has been identified in many different types of solid tumors. These TSC, which are typically more resistant to chemotherapy and radiation compared to other tumor cells, have properties similar to normal stem cells including multipotency and the ability to self-renew, proliferate, and maintain the neoplastic clone. Much of the research on TSC has focused on adult cancers. With considerable differences in tumor biology between adult and pediatric cancers, there may be significant differences in the presence, function and behavior of TSC in pediatric malignancies. We discuss what is currently known about pediatric solid TSC with specific focus on TSC markers, tumor microenvironment, signaling pathways, therapeutic resistance and potential future therapies to target pediatric TSC.

No MeSH data available.


Related in: MedlinePlus

The CD133+ glioma stem cells in the pediatric GBM xenograft D456MG were significantly more sensitive to killing than several adult GBM xenografts tested after 72 hours of low dose infection (1 plaque-forming unit (PFU) per cell) with G207, an engineered herpes simplex virus used in adult GBM trials at the University of Alabama at Birmingham.
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f4-cancers-03-00298: The CD133+ glioma stem cells in the pediatric GBM xenograft D456MG were significantly more sensitive to killing than several adult GBM xenografts tested after 72 hours of low dose infection (1 plaque-forming unit (PFU) per cell) with G207, an engineered herpes simplex virus used in adult GBM trials at the University of Alabama at Birmingham.

Mentions: Another potential method to eradicate pediatric TSC is utilizing mechanisms of cell killing that differ from current conventional therapies. Oncolytic virotherapy is one of these novel approaches. Oncolytic viruses typically work in two main ways: as a direct, targeted attack by containing mutations that cause the virus to spare normal cells but infect tumor cells that then die and release infectious virus to neighboring tumor cells, or by expressing therapeutic foreign gene products that either directly or indirectly lead to cell death. The potential therapeutic benefit of virotherapy in treating pediatric malignancies and the effects of virotherapy on TSC, including pediatric tumors, have been studied in a number of viruses including herpes simplex virus (HSV), adenovirus, myxoma virus, reovirus, and vesicular stomatitis virus [110,111]. We found that the TSC from a pediatric GBM xenograft were more sensitive to killing by engineered HSV than several adult GBM tested (Figure 4) [112]. Cripe's lab showed that an engineered HSV effectively targeted and killed chemoresistant CD133+ neuroblastoma cells [42]. These studies suggest oncolytic virotherapy may be a useful alternative approach to kill resilient TSC. Reversing TSC resistance mechanism by blocking ABC transporters that efflux cytotoxic drugs, for example, or promoting differentiation of TSC to more susceptible tumor cells are additional alternative strategies that have not been specifically examined in pediatric solid tumors and require further study [18].


Cancer Stem Cells and Pediatric Solid Tumors.

Friedman GK, Gillespie GY - Cancers (Basel) (2011)

The CD133+ glioma stem cells in the pediatric GBM xenograft D456MG were significantly more sensitive to killing than several adult GBM xenografts tested after 72 hours of low dose infection (1 plaque-forming unit (PFU) per cell) with G207, an engineered herpes simplex virus used in adult GBM trials at the University of Alabama at Birmingham.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3050504&req=5

f4-cancers-03-00298: The CD133+ glioma stem cells in the pediatric GBM xenograft D456MG were significantly more sensitive to killing than several adult GBM xenografts tested after 72 hours of low dose infection (1 plaque-forming unit (PFU) per cell) with G207, an engineered herpes simplex virus used in adult GBM trials at the University of Alabama at Birmingham.
Mentions: Another potential method to eradicate pediatric TSC is utilizing mechanisms of cell killing that differ from current conventional therapies. Oncolytic virotherapy is one of these novel approaches. Oncolytic viruses typically work in two main ways: as a direct, targeted attack by containing mutations that cause the virus to spare normal cells but infect tumor cells that then die and release infectious virus to neighboring tumor cells, or by expressing therapeutic foreign gene products that either directly or indirectly lead to cell death. The potential therapeutic benefit of virotherapy in treating pediatric malignancies and the effects of virotherapy on TSC, including pediatric tumors, have been studied in a number of viruses including herpes simplex virus (HSV), adenovirus, myxoma virus, reovirus, and vesicular stomatitis virus [110,111]. We found that the TSC from a pediatric GBM xenograft were more sensitive to killing by engineered HSV than several adult GBM tested (Figure 4) [112]. Cripe's lab showed that an engineered HSV effectively targeted and killed chemoresistant CD133+ neuroblastoma cells [42]. These studies suggest oncolytic virotherapy may be a useful alternative approach to kill resilient TSC. Reversing TSC resistance mechanism by blocking ABC transporters that efflux cytotoxic drugs, for example, or promoting differentiation of TSC to more susceptible tumor cells are additional alternative strategies that have not been specifically examined in pediatric solid tumors and require further study [18].

Bottom Line: Recently, a subpopulation of cells, termed tumor-initiating cells or tumor stem cells (TSC), has been identified in many different types of solid tumors.Much of the research on TSC has focused on adult cancers.With considerable differences in tumor biology between adult and pediatric cancers, there may be significant differences in the presence, function and behavior of TSC in pediatric malignancies.

View Article: PubMed Central - PubMed

Affiliation: Division of Pediatric Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.

ABSTRACT
Recently, a subpopulation of cells, termed tumor-initiating cells or tumor stem cells (TSC), has been identified in many different types of solid tumors. These TSC, which are typically more resistant to chemotherapy and radiation compared to other tumor cells, have properties similar to normal stem cells including multipotency and the ability to self-renew, proliferate, and maintain the neoplastic clone. Much of the research on TSC has focused on adult cancers. With considerable differences in tumor biology between adult and pediatric cancers, there may be significant differences in the presence, function and behavior of TSC in pediatric malignancies. We discuss what is currently known about pediatric solid TSC with specific focus on TSC markers, tumor microenvironment, signaling pathways, therapeutic resistance and potential future therapies to target pediatric TSC.

No MeSH data available.


Related in: MedlinePlus