As group leader at St. Anna Children’s Cancer Research Institute (CCRI) in Vienna, Austria, for which he also served as its overall scientific director from 2001 to 2017, Dr. Kovar has been exploring the molecular biology of Ewing sarcoma and its functional and clinical implications for more than 35 years. He studied at the University of Vienna zoology and chemistry and obtained his degree in Molecular Biology in 1984.
After his postdoctoral training at the Medical University of Vienna, he joined a small charity, St. Anna Kinderkrebsforschung to help building the first research institute in Europe entirely dedicated to the study of childhood cancer in 1988, closely affiliated with St. Anna Kinderspital, Austria´s biggest pediatric cancer treatment center. Under his leadership, the CCRI grew to one of Europe´s leading scientific institutions in the field. Being affected by a case of Ewing sarcoma in his close family, Dr. Kovar realized the many unmet needs of this deadly disease early on in his career. He has therefore focused his research on Ewing sarcoma and has made several seminal discoveries on the molecular biology driving Ewing sarcoma pathogenesis.
As cancer in children and adolescents are rare, Dr. Kovar strongly believes in international multi-disciplinary team science strategies to accelerate ground-breaking discoveries and their translation to the benefit of the patients. Dr. Kovar has been playing a leading role in building a Ewing sarcoma research community across borders and continents.
Over the years, he has engaged with his research group in 9 European collaborative projects and most recently has led an ALSF Crazy 8 team to uncover the origins of Ewing sarcoma. Finally, Dr. Kovar has contributed to the training of the next generation of pediatric cancer researchers by supervising a large number of PhD theses, contributing to a Marie Sklodowska-Curie European Training Network, and as a teacher at the Medical University of Vienna. His current research interests include understanding the developmental engine to model Ewing sarcoma pathogenesis, causes and consequences of tumor cell plasticity, and reverse engineering and targeting metastatic niche-mimicking tumor microenvironments and gene regulatory networks.
