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Open Access 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

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

Published: 23 January 2013

Abstract

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.

Keywords:
Cancer; Lymphocyte; Metabolism; Aerobic glycolysis