近日,，得克薩斯大學西南醫(yī)學中心研究人員在Nature雜志上發(fā)表研究論文揭示了為何最常見的致命的腦腫瘤在成人中會復發(fā),，并發(fā)現(xiàn)了未來治療的潛在靶點,。
膠質母細胞瘤（GBM）,，目前被認為是不治之癥,。盡管初始能接受治療,，但這種癌癥類型幾乎總是會復發(fā),。GBM發(fā)病率是一個快速增長的腫瘤類型。
根據國家癌癥研究所的數據證實這種惡性腦瘤存活率中位數是大約15個月,。
Luis Parada博士說：我們發(fā)現(xiàn)了一類增長較慢或保持靜止狀態(tài)的腦腫瘤細胞,，這類細胞似乎是接受標準治療藥物Temozolomide后癌癥復發(fā)的最主要原因,。
使用GBM遺傳工程小鼠模型，研究人員發(fā)現(xiàn)靜息的腫瘤細胞具有干細胞樣行為,，干細胞樣腫瘤細胞會一直處于靜息狀態(tài)直到被激活,。
Parada博士說：在實體腫瘤組織中癌癥干細胞的存在仍然是有爭議的，我們正在努力更好地了解這些細胞,，目前我們現(xiàn)在正面臨著的是技術上的障礙,，而不是概念上的困擾。（生物谷：Bioon.com）
編譯自：Study suggests new treatment target for glioblastoma multiforme
doi:10.1038/nature11287
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PMID:
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
Glioblastoma multiforme is the most common primary malignant brain tumour, with a median survival of about one year1. 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.
