重编程
胰腺癌
癌症研究
生物
细胞生物学
PI3K/AKT/mTOR通路
癌细胞
生物信息学
癌症
细胞
遗传学
信号转导
作者
Jorge Franco,Uthra Balaji,Elizaveta Freinkman,Agnieszka K. Witkiewicz,Erik S. Knudsen
出处
期刊:Cell Reports
[Cell Press]
日期:2020-07-01
卷期号:32 (1): 107793-107793
被引量:7
标识
DOI:10.1016/j.celrep.2020.107793
摘要
(Cell Reports 14, 979–990; February 9, 2016) In the originally published version of this article, there was an inadvertent duplication of the single agent controls in Figure 1E. A corrected version of the figure panel is provided here. The authors regret this error. Metabolic Reprogramming of Pancreatic Cancer Mediated by CDK4/6 Inhibition Elicits Unique VulnerabilitiesFranco et al.Cell ReportsJanuary 21, 2016In BriefCDK4/6 inhibitors are potent inhibitors of cell cycle that are employed clinically. Franco et al. report that the inhibition of CDK4/6 in pancreatic cancer models reprograms metabolism through a pathway involving the RB tumor suppressor and MTOR activation. These findings demonstrate specific metabolic adaptations to this class of therapeutic agents and delineate vulnerabilities for future therapeutic intervention. Full-Text PDF Open Access
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