Stopping anti-CCL2 breast cancer treatment aggravates the disease

Mohamed Bentires-Alj and his team at the Friedrich Miescher Institute for Biomedical Research (FMI) together with scientists from the Novartis Institutes for BioMedical Research (NIBR) show in a study that a promising therapeutic approach for metastatic breast cancer elicits deleterious effects after cessation of the treatment. Stopping CCL2 inhibition paradoxically increases metastasis formation and leads to premature death thus thwarting the initially beneficial effects of the treatment. This has implications for the design of therapies targeting these processes and indicates that therapeutic approaches to inactivate the chemokine CCL2 should be administered with extreme caution. The majority of breast-cancer-related-deaths are still caused by metastases. The formation of metastasis as well as tumor growth are influenced by the dynamic interplay between the cells surrounding a tumor (the so called tumor microenvironment) and the tumor cells themselves. 'Understanding the cellular and molecular mechanisms underlying the interplay between cancer cells and the tumor microenvironment is of paramount importance. Only by understanding mechanisms of cancer, we will pinpoint efficacious and long lasting treatments' said Bentires-Alj.