Nuclear Receptor Tyrosine Kinases Mediating Chromatin Remodeling & Checkpoint Adaption
Background
Rhabdomyosarcoma is the most common soft tissue sarcoma of childhood and adolescence. The alveolar subtype is noticeably more aggressive than the embryonal subtype of rhabdomyosarcoma. This disease often responds to chemotherapy, but in many patients the available treatments fail – a deadly outcome. We identified how a cancer-causing fusion gene called Pax3:Foxo1 may lead to treatment failure: by turning on growth factor genes late in the process of tumor cell duplication. We believe this pro-growth, pro-survival process allows tumor cells to endure chemotherapy and radiation and allow tumor recurrences.
Project Goals
We want to determine if FGFR1 (a growth factor related to Pax3:Foxo1) is a suitable target for drug development for children with alveolar rhabdomyosarcoma and will help limit treatment resistance in tumor cells.
