Abstract
The cellular origins and the mechanisms of progression, maintenance of tumorigenicity, and therapeutic resistance are central questions in the glioblastoma multiforme (GBM) field. Using tumor suppressor mouse models, our group recently reported two independent populations of adult GBM-initiating central nervous system progenitors. We found different functional and molecular subtypes depending on the tumor-initiating cell lineage, indicating that the cell of origin is a driver of GBMsubtype diversity. Using an in vivo model, we also showed that GBM cancer stem cells (CSCs) or glioma stem cells (GSCs) contribute to resistance to chemotherapeutic agents and that genetic ablation of GSCs leads to a delay in tumor progression. These studies are consistent with the cell of origin and CSCs as critical regulators of the pathogenesis of GBM.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 31-36 |
| Number of pages | 6 |
| Journal | Cold Spring Harbor Symposia on Quantitative Biology |
| Volume | 81 |
| Issue number | 1 |
| DOIs | |
| State | Published - 2016 |
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ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Genetics
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Cell of origin and cancer stem cells in tumor suppressor mouse models of glioblastoma. / Alcantara Llaguno, Sheila R.; Xie, Xuanhua; Parada, Luis F.
In: Cold Spring Harbor Symposia on Quantitative Biology, Vol. 81, No. 1, 2016, p. 31-36.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cell of origin and cancer stem cells in tumor suppressor mouse models of glioblastoma
AU - Alcantara Llaguno, Sheila R.
AU - Xie, Xuanhua
AU - Parada, Luis F.
PY - 2016
Y1 - 2016
N2 - The cellular origins and the mechanisms of progression, maintenance of tumorigenicity, and therapeutic resistance are central questions in the glioblastoma multiforme (GBM) field. Using tumor suppressor mouse models, our group recently reported two independent populations of adult GBM-initiating central nervous system progenitors. We found different functional and molecular subtypes depending on the tumor-initiating cell lineage, indicating that the cell of origin is a driver of GBMsubtype diversity. Using an in vivo model, we also showed that GBM cancer stem cells (CSCs) or glioma stem cells (GSCs) contribute to resistance to chemotherapeutic agents and that genetic ablation of GSCs leads to a delay in tumor progression. These studies are consistent with the cell of origin and CSCs as critical regulators of the pathogenesis of GBM.
AB - The cellular origins and the mechanisms of progression, maintenance of tumorigenicity, and therapeutic resistance are central questions in the glioblastoma multiforme (GBM) field. Using tumor suppressor mouse models, our group recently reported two independent populations of adult GBM-initiating central nervous system progenitors. We found different functional and molecular subtypes depending on the tumor-initiating cell lineage, indicating that the cell of origin is a driver of GBMsubtype diversity. Using an in vivo model, we also showed that GBM cancer stem cells (CSCs) or glioma stem cells (GSCs) contribute to resistance to chemotherapeutic agents and that genetic ablation of GSCs leads to a delay in tumor progression. These studies are consistent with the cell of origin and CSCs as critical regulators of the pathogenesis of GBM.
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U2 - 10.1101/sqb.2016.81.030973
DO - 10.1101/sqb.2016.81.030973
M3 - Article
VL - 81
SP - 31
EP - 36
JO - Cold Spring Harbor Symposia on Quantitative Biology
JF - Cold Spring Harbor Symposia on Quantitative Biology
SN - 0091-7451
IS - 1
ER -