Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction

被引：1366

作者：

Luo, Ji ^{[1
]}

Solimini, Nicole L. ^{[1
]}

Elledge, Stephen J. ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Howard Hughes Med Inst,Dept Med,Div Genet,Dept Ge, Boston, MA 02115 USA

来源：

CELL | 2009年 / 136卷 / 05期

关键词：

DNA-DAMAGE RESPONSE; GROWTH-FACTOR RECEPTOR; HUMAN BREAST; NEOPLASTIC PHENOTYPE; GENOMIC INSTABILITY; SIGNALING PATHWAYS; MITOTIC CHECKPOINT; INDUCED SENESCENCE; RNA INTERFERENCE; P53; RESTORATION;

D O I：

10.1016/j.cell.2009.02.024

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Cancer is a complex collection of distinct genetic diseases united by common hallmarks. Here, we expand upon the classic hallmarks to include the stress phenotypes of tumorigenesis. We describe a conceptual framework of how oncogene and non-oncogene addictions contribute to these hallmarks and how they can be exploited through stress sensitization and stress overload to selectively kill cancer cells. In particular, we present evidence for a large class of non-oncogenes that are essential for cancer cell survival and present attractive drug targets. Finally, we discuss the path ahead to therapeutic discovery and provide theoretical considerations for combining orthogonal cancer therapies.

引用

页码：823 / 837

页数：15

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