Dr. De Raedt researches pediatric high grade glioma development and aims to understand the involvement of crucial pathways. He investigates pathway interaction, and explores ways to develop therapies through analyzing human tumors, performing cellular studies, and developing accurate mouse models. This allows Dr. De Raedt and his team to perform novel pre-clinical studies that can lead to clinical trials.
Dr. Bhoj's genetics research aims to discover new human disease genes, their mechanisms, and potential targeted therapies. In addition to ongoing gene discovery efforts, Dr. Bhoj focuses on three novel genes that lead to pediatric neurologic dysfunction: TBC1 domain-containing kinase, Histone 3.3 (H3F3A and H3F3B), and MAP4K4.
John Maris, MD, distinguished neuroblastoma researcher at CHOP, received the the National Cancer Institute's prestigious Outstanding Investigator Award.
An international collaboration of researchers has identified several progressive series of mutations that occur in tumor cells responsible for aggressive subsets of neuroblastoma that relapse after chemotherapy.
Research in the De Raedt Lab centers on pediatric high-grade glioma development and aims to understand the involvement of crucial pathways that drive these pediatric brain tumors. The lab investigates pathways interaction, and it explores ways to develop therapies through analyzing human tumors, performing cellular studies, and developing accurate mouse models. This allows the lab team to perform novel preclinical studies that can lead to clinical trials.
The Mossé Laboratory studies the role of the anaplastic lymphoma kinase (ALK) oncogene in the initiation and progression of neuroblastoma, with a focus on developing innovative therapeutic strategies for patients with this often lethal disease.
The Bhoj Lab is a genetics lab that discovers new human disease genes, their mechanisms, and potential targeted therapies. In addition to ongoing gene discovery efforts, the lab focuses on three novel genes that lead to pediatric neurologic dysfunction: TBCK, H3F3A/B, and MAP4K4.
