Email updates

Keep up to date with the latest news and content from Cancer & Metabolism and BioMed Central.

Open Access Highly Accessed Open Badges Review

Activated lymphocytes as a metabolic model for carcinogenesis

Andrew N Macintyre and Jeffrey C Rathmell*

Author Affiliations

Department of Pharmacology and Cancer Biology, Department of Immunology, Sarah W. Stedman Nutrition and Metabolism Center, Duke University, Durham, NC, 27710, USA

For all author emails, please log on.

Cancer & Metabolism 2013, 1:5  doi:10.1186/2049-3002-1-5

Published: 23 January 2013


Metabolic reprogramming is a key event in tumorigenesis to support cell growth, and cancer cells frequently become both highly glycolytic and glutamine dependent. Similarly, T lymphocytes (T cells) modify their metabolism after activation by foreign antigens to shift from an energetically efficient oxidative metabolism to a highly glycolytic and glutamine-dependent metabolic program. This metabolic transition enables T cell growth, proliferation, and differentiation. In both activated T cells and cancer cells metabolic reprogramming is achieved by similar mechanisms and offers similar survival and cell growth advantages. Activated T cells thus present a useful model with which to study the development of tumor metabolism. Here, we review the metabolic similarities and distinctions between activated T cells and cancer cells, and discuss both the common signaling pathways and master metabolic regulators that lead to metabolic rewiring. Ultimately, understanding how and why T cells adopt a cancer cell-like metabolic profile may identify new therapeutic strategies to selectively target tumor metabolism or inflammatory immune responses.

Cancer; Lymphocyte; Metabolism; Aerobic glycolysis