Oren J Becher, MD
Associate Professor, Pediatrics; Feinberg School of Medicine
With the recent discovery of H3.3/H3.1 K27M and ACVR1/ALK2 mutations in DIPG, there is a need to understand the mechanism by which these mutations contribute to DIPG pathogenesis. Towards that goal, we has developed genetically engineered mouse models (GEMMs) that incorporate these novel oncogenes and we are using these models to dissect the mechanisms by which these oncoproteins contribute to brainstem gliomagenesis as well as evaluate novel therapeutics. Novel insights regarding these oncoproteins gleaned from our studies with the GEMMs will be validated in human DIPG models that harbor these oncogenes.