Targeting cancer metabolism: a therapeutic window opens

被引：1173

作者：

Vander Heiden, Matthew G. ^{[1
,2
,3
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机构：

[1] MIT, Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA

[2] MIT, Dept Biol, Cambridge, MA 02139 USA

[3] Dana Farber Canc Inst, Boston, MA 02115 USA

来源：

NATURE REVIEWS DRUG DISCOVERY | 2011年 / 10卷 / 09期

基金：

美国国家卫生研究院;

关键词：

TUMOR-CELL GROWTH; INTEGRATED GENOMIC ANALYSIS; FATTY-ACID SYNTHASE; PYRUVATE-KINASE M2; ATP CITRATE LYASE; GLUTAMINE-METABOLISM; BREAST-CANCER; GLUCOSE-METABOLISM; NICOTINAMIDE PHOSPHORIBOSYLTRANSFERASE; ONCOMETABOLITE; 2-HYDROXYGLUTARATE;

D O I：

10.1038/nrd3504

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Genetic events in cancer activate signalling pathways that alter cell metabolism. Clinical evidence has linked cell metabolism with cancer outcomes. Together, these observations have raised interest in targeting metabolic enzymes for cancer therapy, but they have also raised concerns that these therapies would have unacceptable effects on normal cells. However, some of the first cancer therapies that were developed target the specific metabolic needs of cancer cells and remain effective agents in the clinic today. Research into how changes in cell metabolism promote tumour growth has accelerated in recent years. This has refocused efforts to target metabolic dependencies of cancer cells as a selective anticancer strategy.

引用

页码：671 / 684

页数：14

共 173 条

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