“We can turn Pax3:Foxo off in Rhabdomyosarcoma”
The Focus On Rhabdo Webinar Series continues on November 15th, 2015 at 2PM Eastern with Dr. Charles Keller. His topic of turning off the Pax3:Foxo fusion gene in aRMS should be of interest to many of us.
Cell of origin of cancers is often unknown and thus is not a consideration in treatment approaches. Alveolar rhabdomyosarcoma (aRMS) is an aggressive childhood cancer for which the cell of origin remains debated. We used genetically-engineered mouse models of aRMS to activate Pax3:Foxo1 fusion oncogene and inactivate the p53 tumor suppressor in several stages of muscle development before and after birth. These studies reveal that cell of origin significantly influences tumor appearance and susceptibility to targeted, non-chemotherapy drugs. Furthermore, this work led us to identify the histone deacetylase inhibitor entinostat as a drug for the potential conversion of Pax3:Foxo1-positive aRMS to a state akin to fusion-negative RMS by directly turning off Pax3:Foxo1.
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