Cancer's sweet tooth

被引：162

作者：

Bui, Thi ^{[1
]}

Thompson, Craig B.

机构：

[1] Univ Penn, Sch Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA

[2] Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA

[3] Univ Penn, Sch Med, Dept Canc Biol, Philadelphia, PA 19104 USA

来源：

CANCER CELL | 2006年 / 9卷 / 06期

关键词：

D O I：

10.1016/j.ccr.2006.05.012

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Even in the presence of an adequate oxygen supply, many tumors metabolize the majority of the glucose they take up through glycolysis. It has been a long-held belief that this glycolytic phenotype is due to cancer-specific defects in mitochondrial oxidative phosphorylation. In this issue of Cancer Cell, Fantin et al. now report that most tumor cells have a substantial reserve capacity to produce ATP by oxidative phosphorylation when glycolysis is suppressed. These new data add to mounting evidence that the high rate of glycolysis exhibited by most tumors is required to support cell growth rather than to compensate for defect(s) in mitochondrial function.

引用

页码：419 / 420

页数：2

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