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胶质瘤形成、癌症干细胞与Akt信号传导

Glioma formation, cancer stem cells, and akt signaling.

作者信息

Hambardzumyan Dolores, Squatrito Massimo, Carbajal Eletha, Holland Eric C

机构信息

Department of Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.

出版信息

Stem Cell Rev. 2008 Sep;4(3):203-10. doi: 10.1007/s12015-008-9021-5.

Abstract

Several recent reports have provided evidence that cancer is initiated by a rare fraction of cells called "cancer stem cells" which are multipotent, self-renewing subset of the tumor. However, several issues regarding the biology and techniques of isolating these cells from solid tumors remain to be clarified. In addition, experimental data supports two possibilities for glioma cell of origin. First, that stem cells or early progenitors are transformed and show variable differentiation of their progeny during tumor development. Second, that more differentiated glia are transformed by genetic events that lead to a loss of differentiation maintenance. In human gliomas, these two theories are not mutually exclusive. In this review we will summarize both theories, and highlight outstanding issues that remain to be resolved.

摘要

最近的几份报告提供了证据,表明癌症是由一小部分称为“癌症干细胞”的细胞引发的,这些细胞是肿瘤中具有多能性、自我更新能力的亚群。然而,关于从实体瘤中分离这些细胞的生物学和技术的几个问题仍有待阐明。此外,实验数据支持胶质瘤细胞起源的两种可能性。第一,干细胞或早期祖细胞发生转化,并在肿瘤发展过程中其后代表现出可变的分化。第二,分化程度更高的神经胶质细胞因导致分化维持丧失的基因事件而发生转化。在人类胶质瘤中,这两种理论并非相互排斥。在这篇综述中,我们将总结这两种理论,并突出仍有待解决的突出问题。

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