Progress against DIPG, a fatal childhood brain tumor, is usually a game of inches. Studies that hint at even small gains are cause for celebration.
That’s why researchers at the University of Michigan and their collaborators are excited about discoveries that point toward a new potential treatment approach — one that significantly lengthened survival times in two mouse models of DIPG.
The team’s findings suggest that simultaneously targeting two energy-production pathways within the cancer cells could help overcome the effects of a cancer-causing mutation that is one of the hallmarks of DIPG, or diffuse intrinsic pontine glioma, and similar tumors.
“DIPGs have a characteristic, epigenetic histone mutation — that is, a mutation in the spool that DNA wraps around, and which can affect gene expression,” says the study’s senior author Sriram Venneti, M.D., Ph.D., a neuropathologist and researcher at the U-M Rogel Cancer Center and Chad Carr Pediatric Brain Tumor Center. “It’s not clear exactly how this mutation causes cancer, but it’s associated with poor outcomes, which implies these mutations are aggressively driving the biology of these tumors.”
