Glioblastoma multiforme is the most common primary malignant brain tumor, with a median survival of about one year. This poor prognosis is due to therapeutic resistance and tumor recurrence after surgical removal. This study identifies a subset of endogenous tumor cells that are the source of new tumor cells after the drug temozolomide (TMZ) is administered to temporarily arrest tumor growth. A transgene called Nes-ΔTK-GFP labels quiescent subventricular zone adult neural stem cells and a subset of endogenous glioma tumor cells. Pulse-chase experiments show that tumor regrowth originates from the Nes-ΔTK-GFP subpopulation. Ablation of GFP+ cells with chronic ganciclovir administration significantly arrests tumor growth, and combined TMZ and ganciclovir treatment impede tumor development. A relatively quiescent subset of endogenous glioma cells, with properties similar to those proposed for cancer stem cells, is responsible for sustaining long-term tumor growth through the production of transient populations of highly proliferative cells. The study used genetically engineered mouse models to investigate the role of neural stem cells in glioma development. The Nes-ΔTK-GFP transgene was used to label quiescent neural stem cells and endogenous glioma cells. GCV treatment effectively ablates quiescent cells, while TMZ targets proliferating cells. TMZ treatment reduced BrdU incorporation in tumors and NSC niches, but tumor recurrence was inevitable. Pulse-chase experiments with BrdU analogues showed that tumor cells after TMZ treatment were primarily derived from GFP+ cells. GCV treatment significantly reduced tumor growth and improved survival. The study also showed that GCV treatment effectively eliminated GFP+ cells, which are quiescent and responsible for tumor growth. The study found that the Nes-ΔTK-GFP transgene labels quiescent cells in the subventricular zone and that these cells are responsible for tumor growth. GCV treatment effectively eliminated these cells, leading to reduced tumor growth and improved survival. The study also showed that TMZ and GCV combination treatment significantly inhibited tumor growth. The study concluded that the quiescent cells, with properties similar to cancer stem cells, are responsible for sustaining tumor growth and recurrence after chemotherapy. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cellsGlioblastoma multiforme is the most common primary malignant brain tumor, with a median survival of about one year. This poor prognosis is due to therapeutic resistance and tumor recurrence after surgical removal. This study identifies a subset of endogenous tumor cells that are the source of new tumor cells after the drug temozolomide (TMZ) is administered to temporarily arrest tumor growth. A transgene called Nes-ΔTK-GFP labels quiescent subventricular zone adult neural stem cells and a subset of endogenous glioma tumor cells. Pulse-chase experiments show that tumor regrowth originates from the Nes-ΔTK-GFP subpopulation. Ablation of GFP+ cells with chronic ganciclovir administration significantly arrests tumor growth, and combined TMZ and ganciclovir treatment impede tumor development. A relatively quiescent subset of endogenous glioma cells, with properties similar to those proposed for cancer stem cells, is responsible for sustaining long-term tumor growth through the production of transient populations of highly proliferative cells. The study used genetically engineered mouse models to investigate the role of neural stem cells in glioma development. The Nes-ΔTK-GFP transgene was used to label quiescent neural stem cells and endogenous glioma cells. GCV treatment effectively ablates quiescent cells, while TMZ targets proliferating cells. TMZ treatment reduced BrdU incorporation in tumors and NSC niches, but tumor recurrence was inevitable. Pulse-chase experiments with BrdU analogues showed that tumor cells after TMZ treatment were primarily derived from GFP+ cells. GCV treatment significantly reduced tumor growth and improved survival. The study also showed that GCV treatment effectively eliminated GFP+ cells, which are quiescent and responsible for tumor growth. The study found that the Nes-ΔTK-GFP transgene labels quiescent cells in the subventricular zone and that these cells are responsible for tumor growth. GCV treatment effectively eliminated these cells, leading to reduced tumor growth and improved survival. The study also showed that TMZ and GCV combination treatment significantly inhibited tumor growth. The study concluded that the quiescent cells, with properties similar to cancer stem cells, are responsible for sustaining tumor growth and recurrence after chemotherapy. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells are. The study also showed that the quiescent cells are not affected by GCV treatment, while proliferating cells