Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion
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- 作者：Kensuke Tateishi1 ; Hiroaki Wakimoto1 ; A. John Iafrate3 ; Shota Tanaka2 ; Franziska Loebel1 ; Nina Lelic1 ; Dmitri Wiederschain5 ; Olivier Bedel5 ; Gejing Deng5 ; Bailin Zhang5 ; Timothy He5 ; Xu Shi6 ; Robert E. Gerszten6 ; Yiyun Zhang6 ; Jing-Ruey J. Yeh6 ; William T. Curry1 ; Dan Zhao2 ; Sudhandra Sundaram2 ; Fares Nigim1 ; Mara V.A. Koerner1 ; Quan Ho3 ; David E. Fisher7 ; Elisabeth M. Roider7 ; Lajos V. Kemeny7 ; Yardena Samuels8 ; Keith T. Flaherty4 ; Tracy T. Batchelor2 ; Andrew S. Chi2 ; 9 ; chia01@nyumc.org" class="auth_mail" title="E-mail the corresponding author ; Daniel P. Cahill1 ; cahill@mgh.harvard.edu" class="auth_mail" title="E-mail the corresponding author
- 刊名：Cancer Cell
- 出版年：2015
- 出版时间：14 December 2015
- 年：2015
- 卷：28
- 期：6
- 页码：773-784
- 全文大小：3475 K
文摘
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Growth of IDH1 mutant cancers can be decoupled from 2-hydroxyglutarate levels
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Mutant IDH1 decreases NAD+ levels by inhibiting an alternate NAD+ salvage pathway
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Depletion of NAD+ is strikingly potent and specific for IDH1 mutant cancers
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NAD+ depletion induces autophagy by activating intracellular energy sensors