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Despite the high cure rates among children with cancer, following treatment with current multimodality therapies, survivors face profound lifelong therapy-related complications. In addition, survival rate for many high-risk pediatric cancer patients had not improved significantly over the last 30 years. Hopes for the future depend on identifying novel therapies that target specific cancer-driving cellular and molecular mechanisms.

Components of the RAS and ERK MAPK pathways are frequently deregulated in pediatric cancers including leukemias, central nervous system tumors, and extracranial solid tumors. Our focus is to systematically define mechanisms of RAS and ERK MAPK- driven vulnerabilities in pediatric cancers and design directions for novel targeted therapies. Toward these efforts we employ a wide variety of in vitro cell-based assays, unbiased genetic and pharmacologic screens as well as in vivo preclinical testing of patient-derived xenograft tumor models.

Another focus of our research is to understand how the two oncogenes RAS and MYC cooperate to promote tumor cell growth and maintenance and how we can exploit this cooperation in order to design therapeutic strategies for RAS-driven pediatric cancers.