Over the last decade, strong evidence has accumulated that the tumor micro-environment plays a key role in recurrence, metastasis and poor clinical outcome in breast cancer patients. In this context, more recent discoveries indicate that catabolic cancer-associated fibroblasts (CAFs) produce nutrients (lactate, ketone bodies and glutamine) to fuel anabolic mitochondrial metabolism in cancer cells. This new paradigm is known as metabolic-symbiosis or metabolic asymmetry and reflects the co-existence of multiple metabolic compartments in a given tumor. This type of metabolic co-operation in the tumor ecosystem underlies the metabolic heterogeneity found in human breast cancers, and can be used to more effectively predict tumor recurrence, metastasis, drug-resistance and poor clinical outcome, in breast cancer patients.

In my talk, I will highlight how this metabolic-symbiosis phenotype could be targeted from a therapeutic point of view, bringing us closer to the goal of personalized medicine.

For further information on this topic, please see the following references:

Caveolae and signalling in cancer.

Martinez-Outschoorn UE, Sotgia F, Lisanti MP.

Nat Rev Cancer. 2015 Apr;15(4):225-37.

Metabolic asymmetry in cancer: A balancing act that promotes tumor growth.

Martinez-Outschoorn UE, Sotgia F, Lisanti MP.

Cancer Cell. 2014 Jul 14;26(1):5-7.

Power surge: Supporting cells fuel cancer cell mitochondria.

Martinez-Outschoorn UE, Sotgia F, Lisanti MP.

Cell Metab. 2012 Jan 4;15(1):4-5.

Citation Format: Lisanti MP. Metabolic asymmetry in breast cancer: Implications for personlised medicine. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr ES2-3.