This project is  developing a pre-clinical model of DIPG that recapitulates the disease that occurs in children. In its first iteration the model incorporated the 2 most common mutations observed in children, which are thought to drive the development of the tumour. These mutations, H3.3 K27M and p53 were genetically introduced into the DNA and switched on after birth by introducing tamoxifen into the drinking water. A reporter gene, also under the control of tamoxifen, was introduced to highlight the area(s) of the brain that express the mutations. The initial iteration of the model did not induce DIPG. The model is now being modified to express the mutations in utero. If successful, the model will be provided to a central repository as a resource for all DIPG researchers. This work is co-funded by Brainchild Foundation.