Adaptive Chromatin Remodeling Drives Glioblastoma Stem Cell Plasticity and Drug Tolerance

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• 作者：Brian B. Liau¹ ; ² ; ⁷ ; Cem Sievers¹ ; ² ; ⁷ ; Laura K. Donohue¹ ; ² ; Shawn M. Gillespie¹ ; ² ; William A. Flavahan¹ ; ² ; Tyler E. Miller⁵ ; ⁶ ; Andrew S. Venteicher¹ ; ² ; ³ ; Christine H. Hebert¹ ; ² ; Christopher D. Carey⁴ ; Scott J. Rodig⁴ ; Sarah J. Shareef¹ ; ² ; Fadi J. Najm¹ ; ² ; Peter van Galen¹ ; ² ; Hiroaki Wakimoto³ ; Daniel P. Cahill³ ; Jeremy N. Rich⁵ ; ⁶ ; Jon C. Aster⁴ ; Mario L. Suvà ; ¹ ; ² ; Anoop P. Patel¹ ; ² ; ³ ; ^{apatel1@uw.edu} ; Bradley E. Bernstein¹ ; ² ; ⁸ ; ^{bernstein.bradley@mgh.harvard.edu}
• 关键词：KDM6A/B ; histone demethylases ; chromatin ; glioblastoma ; drug resistance ; cancer ; epigenetics ; Notch ; stem cell
• 刊名：Cell Stem Cell
• 出版年：2017
• 出版时间：2 February 2017
• 年：2017
• 卷：20
• 期：2
• 页码：233-246.e7
• 全文大小：3708 K
• 卷排序：20

文摘

GSCs can become drug-tolerant and persister-like following RTK inhibitor exposure Persister GSCs exhibit NSC-like programs and are sustained by Notch signaling Notch-high, slow-cycling GSCs are found in primary GBM tumors Persister GSCs reorganize their repressive chromatin and are dependent on KDM6