Discovering the role of titin (TTN) in anthracycline-induced cardiac dysfunction in breast cancer.
Discovering the role of titin (TTN) in anthracycline-induced cardiac dysfunction in cancer patients.
Anthracyclines are the mainstay of chemotherapeutic treatment in a wide range of malignancies, including breast cancer and blood cancers such as leukemia and lymphoma. Due to a growing population of cancer-survivors, the importance of long-term complications of anti-cancer treatment has increased. The most important side effect of anthracycline is cardiac toxicity and today's cancer patients may become tomorrow's heart failure patients. There is an important inter individual susceptibility for the development of cardiotoxicity. This variation is not fully explained by differences in known risk factors. Therefore, it is suggested that genetic variations may play a role. It was recently shown that genetic variants in titin, an import anchoring protein in the cardiomyocytes, can cause a predisposition to dilated cardiomyopathies that are clinically similar to chemotherapy-induced cardiotoxicity In this research project we aim to investigate whether mutations in important structural cardiac genes, more specific titin, can cause an increased susceptibility for cardiotoxicity.
Funding: FWO
Researcher: Boen Hanne
Promotor: Van Craenenbroeck Emeline
Co-promotor: Heidbuchel Hein
Co-promotor: Loeys Bart
Co-promotor: Maaike Alaerts