Pancreatic Cancer Metabolism: Breaking It Down to Build It Back Up

被引:164
作者
Perera, Rushika M. [1 ,2 ,3 ]
Bardeesy, Nabeel [1 ,2 ,3 ]
机构
[1] Massachusetts Gen Hosp, Ctr Canc Res, Boston, MA 02114 USA
[2] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA
[3] Harvard Univ, Sch Med, Dept Med, Boston, MA USA
关键词
BODY-MASS INDEX; DUCTAL ADENOCARCINOMA; ONCOGENIC KRAS; TRANSCRIPTIONAL CONTROL; LACTATE-DEHYDROGENASE; LYSOSOMAL BIOGENESIS; INSULIN-RESISTANCE; OXIDATIVE STRESS; TUMOR-GROWTH; FATTY-ACIDS;
D O I
10.1158/2159-8290.CD-15-0671
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
How do cancer cells escape tightly controlled regulatory circuits that link their proliferation to extracellular nutrient cues? An emerging theme in cancer biology is the hijacking of normal stress response mechanisms to enable growth even when nutrients are limiting. Pancreatic ductal adenocarcinoma (PDA) is the quintessential aggressive malignancy that thrives in nutrient-poor, hypoxic environments. PDAs overcome these limitations through appropriation of unorthodox strategies for fuel source acquisition and utilization. In addition, the interplay between evolving PDA and whole-body metabolism contributes to disease pathogenesis. Deciphering how these pathways function and integrate with one another can reveal novel angles of therapeutic attack. Significance: Alterations in tumor cell and systemic metabolism are central to the biology of pancreatic cancer. Further investigation of these processes will provide important insights into how these tumors develop and grow, and suggest new approaches for its detection, prevention, and treatment. (C) 2015 AACR.
引用
收藏
页码:1247 / 1261
页数:15
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