Although advancements in breast cancer detection and treatment have greatly improved patient outcomes, relapse from the disease is still a leading cause of cancer-related death in women. Recurrent breast tumors typically originate from a subpopulation of cancer cells that survive therapeutic interventions, and they are difficult to identify prior to relapse because they escape cancer therapy through adaptations that help them behave like normal cells.

A research team led by Martin Jechlinger, PhD, at the European Molecular Biology Laboratory in Heidelberg, Germany, examined gene transcription profiles and metabolism pathways in human breast cancer tumors and in mouse models of breast cancer (J Clin Invest 2017; doi:10.1172/JCI89914). They discovered residual tumor cells display alterations in gene transcription and metabolism that affect how the cells synthesize and store fats. Changes in fat metabolism were coupled to increases in oxidative stress and DNA damage, suggesting residual cancer cells rely on these metabolic adaptations to acquire the mutations that trigger cancer relapse.

The researchers then examined pre- and post-treatment biopsies from breast cancer patients and, consistent with their previous findings, they discovered post-treatment cells exhibited alterations in fat metabolism pathways. These findings provide important insights into the potential of targeting metabolic pathways in residual breast cancer cells as a strategy to prevent relapse.