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.
N1 - Funding Information:
This work was supported in part by Children's Tumor Foundation Young Investigator Award and National In-stitutes of Health (NIH) T32 Postdoctoral Trainee support (2T32CA124334-06; PI: Jerry Shay) to S.R.A.L. X.X. is supported by the American Brain Tumor Association Fellowship. L.F.P. is an American Cancer Society Research Professor and recipient of NIH R01 grant CA131313-01A1 and Cancer Prevention and Research Institute of Texas Grant RP100782.
Publisher Copyright:
© 2016 Alcantara Llaguno et al.
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
C2 - 27815542
AN - SCOPUS:85021007355
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 -