The Cristian Rivera Foundation has pledged its support to Dr. Mark Souweidane and Dr. Oren Becher as they execute their important research and clinical trials to help end DIPG and other rare forms of pediatric brain cancer.
In 2012, Dr. Mark Souweidane, the Director of the Pediatric Brain and Spine Center at Weill Cornell Medical Center and Memorial Sloan Kettering, officially launched a pioneering clinical trial that would test the safety of a highly innovative approach using a small fiber to directly deliver drugs into the tumor. On May 1st of that year, the date of his first official surgery, Dr. Souweidane said with pride, “Today, is the first day of Brain Tumor Awareness Month. It marks a day of hope for her family, an entry into a new treatment approach for these children, and the culmination of over 15 years of translational research.”
To describe the goal of the clinical trial, Dr. Souweidane said, “[My colleagues and I] have designed a treatment option for children with DIPG that uses Convection-Enhanced Delivery (CED) and a tumor specific agent called a monoclonal antibody. The drug delivery method of CED bypasses the blood-brain barrier (BBB), a structural interface that isolates the brain from the blood. This delivery method has the dual potential benefit of getting high therapeutic doses of drugs into the tumor while totally avoiding any systemic exposure or toxicity.”
Complementing Dr. Souweidane’s amazing work is the enlightening research being performed at the Ann & Robert H. Lurie Children’s Hospital and the Lurie Cancer center at Northwestern University lab of Dr. Oren Becher. The Cristian Rivera Foundation is proud to support Dr. Becher, helping him and his team develop genetic models of DIPG to better understand the function of genetic alterations in DIPG formation, specifically the genetic alterations that are most important to inhibit therapeutically.
To explain his research efforts, Dr. Becher said, “Recently, we and others have co-discovered an abnormal cell surface receptor called ACVR1, found in the tumors of a quarter of patients with DIPG, which promotes DIPG tumor growth. We developed a new model that incorporates this abnormal ACVR1 and we are currently trying to understand how it contributes to DIPG as well as determine whether ACVR1 inhibitors are a good idea to treat DIPG. In addition, we are continuing to study a particular mutation in a histone gene that has been identified in the majority of human DIPGs and looking for ways to target it. With regards to the translation of novel agents into clinical trials, we have translated a CDK4-6 inhibitor into a clinical trial for children with recurrent brain tumors through the PBTC. This is the first time that this class of drugs is being evaluated in children with brain tumors.”