Molecular mechanisms of cancer development in obesity

被引：667
作者：
Khandekar, Melin J. [1 ,2 ,3 ]
Cohen, Paul [1 ,2 ,4 ]
Spiegelman, Bruce M. [1 ,2 ]
机构：
[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA
[3] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA
[4] Brigham & Womens Hosp, Div Cardiovasc Med, Boston, MA 02115 USA
来源：
NATURE REVIEWS CANCER | 2011年 / 11卷 / 12期
关键词：
TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR-I; BODY-MASS INDEX; PLASMINOGEN-ACTIVATOR INHIBITOR-1; HUMAN BREAST-CANCER; FATTY-ACID SYNTHASE; INDUCED INSULIN-RESISTANCE; GASTRIC BYPASS-SURGERY; MESENCHYMAL STEM-CELLS; PLASMA C-PEPTIDE;
D O I：
10.1038/nrc3174
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
The increasing incidence of obesity and its co-morbid conditions poses a great challenge to global health. In addition to cardiovascular disease and diabetes, epidemiological data demonstrate a link between obesity and multiple types of cancer. The molecular mechanisms underlying how obesity causes an increased risk of cancer are poorly understood. Obesity disrupts the dynamic role of the adipocyte in energy homeostasis, resulting in inflammation and alteration of adipokine (for example, leptin and adiponectin) signalling. Additionally, obesity causes secondary changes that are related to insulin signalling and lipid deregulation that may also foster cancer development. Understanding these molecular links may provide an avenue for preventive and therapeutic strategies to reduce cancer risk and mortality in an increasingly obese population.
引用
收藏
页码：886 / 895
页数：10
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