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A restricted cell population propagates glioblastoma growth after chemotherapy

机译：化疗后，受限制的细胞群会传播胶质母细胞瘤生长

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摘要

在一个成胶质细胞瘤小鼠模型中，Luis Paradarn及其同事利用在神经干细胞(肿瘤就是在这些rn细胞中出现的)中选择性表达的一种绿色荧光rn蛋白(GFP)“报告蛋白”(repor（er proteirl)，rn来在一个内生环境中追踪癌细胞。该“报告蛋rn白”标记了一小类神经胶质瘤细胞，它们的增rn殖能力没有大部分肿瘤细胞那么强。然而，这rn些GFP~+ 细胞却造成用细胞毒性药物“替莫唑rn胺”治疗后肿瘤的再生。GFP~+细胞的选择性清rn除同时配合“替莫唑胺”治疗对抑制肿瘤生长rn更有效。GFP~+细胞似乎处在癌细胞功能性层rn级的最高端，所以可能代表着癌症干细胞——rn能够维持肿瘤生长的-类肿瘤细胞。以这一类rn癌细胞和增殖能力更强的大部分癌细胞同时作rn为治疗目标，也许能导致更好的治疗效果。%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-ΔTKIRES-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-JTK-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.
机译：在一个成胶质细胞瘤小鼠模型中，Luis Paradarn及其同事利用在神经干细胞(肿瘤就是在这些rn细胞中出现的)中选择性表达的一种绿色荧光rn蛋白(GFP)“报告蛋白”(repor（er proteirl)，rn来在一个内生环境中追踪癌细胞。该“报告蛋rn白”标记了一小类神经胶质瘤细胞，它们的增rn殖能力没有大部分肿瘤细胞那么强。然而，这rn些GFP~+ 细胞却造成用细胞毒性药物“替莫唑rn胺”治疗后肿瘤的再生。GFP~+细胞的选择性清rn除同时配合“替莫唑胺”治疗对抑制肿瘤生长rn更有效。GFP~+细胞似乎处在癌细胞功能性层rn级的最高端，所以可能代表着癌症干细胞——rn能够维持肿瘤生长的-类肿瘤细胞。以这一类rn癌细胞和增殖能力更强的大部分癌细胞同时作rn为治疗目标，也许能导致更好的治疗效果。%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-ΔTKIRES-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-JTK-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.

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  • 来源
    《Nature》 |2012年第7412期|p.522-526419|共6页
  • 作者

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

  • 作者单位

    Department of Developmental Biology & Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA;

    Department of Developmental Biology & Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA;

    Department of Developmental Biology & Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA,Department of Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA,Department of Pathology and Cell Biology, Columbia University, New York, New York 10032, USA;

    Department of Developmental Biology & Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA;

    Department of Pathology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA;

    Department of Developmental Biology & Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA,Department of Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA,Department of Pathology and Cell Biology, Columbia University, New York, New York 10032, USA;

    Department of Developmental Biology & Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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