Transcriptional Addiction in Cancer

被引：1006

作者：

Bradner, James E. ^{[1
]}

Hnisz, Denes ^{[2
]}

Young, Richard A. ^{[2
,3
]}

机构：

[1] Novartis Inst Biomed Res, 181 Massachusetts Ave, Cambridge, MA 02139 USA

[2] Whitehead Inst Biomed Res, 9 Cambridge Ctr, Cambridge, MA 02142 USA

[3] MIT, Dept Biol, 77 Massachusetts Ave, Cambridge, MA 02139 USA

来源：

CELL | 2017年 / 168卷 / 04期

基金：

奥地利科学基金会;

关键词：

ACUTE PROMYELOCYTIC LEUKEMIA; BET BROMODOMAIN INHIBITION; ACUTE LYMPHOBLASTIC-LEUKEMIA; COVALENT CDK7 INHIBITOR; NEGATIVE BREAST-CANCER; MLL-FUSION LEUKEMIA; CELL IDENTITY GENES; RNA-POLYMERASE-II; SUPER-ENHANCER; C-MYC;

D O I：

10.1016/j.cell.2016.12.013

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Cancer arises from genetic alterations that invariably lead to dysregulated transcriptional programs. These dysregulated programs can cause cancer cells to become highly dependent on certain regulators of gene expression. Here, we discuss how transcriptional control is disrupted by genetic alterations in cancer cells, why transcriptional dependencies can develop as a consequence of dysregulated programs, and how these dependencies provide opportunities for novel therapeutic interventions in cancer.

引用

页码：629 / 643

页数：15

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