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A restricted cell population propagates glioblastoma growth after chemotherapy

Jian Chen; Yanjiao Li; Tzong-Shiue Yu; Renée M. McKay; Dennis K. Burns; Steven G. Kernie; Luis F. Parada

(Profiled Authors: Dennis K Burns; Renee M McKay; Luis F Parada)

Nature. 2012;488(7412):522-526.

Abstract

Glioblastoma multiforme is the most common primary malignant brain tumour, with a median survival of about one year. This poor prognosis is due to therapeutic resistance and tumour recurrence after surgical removal. Precisely how recurrence occurs is unknown. Using a genetically engineered mouse model of glioma, here we identify a subset of endogenous tumour cells that are the source of new tumour cells after the drug temozolomide (TMZ) is administered to transiently arrest tumour growth. A nestin-δTK-IRES-GFP (Nes-δTK-GFP) transgene that labels quiescent subventricular zone adult neural stem cells also labels a subset of endogenous glioma tumour cells. On arrest of tumour cell proliferation with TMZ, pulse-chase experiments demonstrate a tumour re-growth cell hierarchy originating with the Nes-δTK-GFP transgene subpopulation. Ablation of the GFP + cells with chronic ganciclovir administration significantly arrested tumour growth, and combined TMZ and ganciclovir treatment impeded tumour development. Thus, a relatively quiescent subset of endogenous glioma cells, with properties similar to those proposed for cancer stem cells, is responsible for sustaining long-term tumour growth through the production of transient populations of highly proliferative cells. © 2012 Macmillan Publishers Limited. All rights reserved.


PMID: 22854781     PMCID: PMC3427400    

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