This research integrates multiomic data to identify a specific, high-risk subtype of Group 3 medulloblastoma characterized by a unique lipid dependency. By analyzing proteomic and metabolic signatures, the authors discovered that MYC-driven tumors rely on the accumulation of lipid droplets to fuel mitochondrial activity and promote cell survival. This metabolic reprogramming creates a targetable vulnerability where the enzyme DGAT1 plays a critical role in managing lipid homeostasis. Experimental evidence demonstrates that inhibiting DGAT1 reduces tumor growth and enhances the effectiveness of chemotherapy in preclinical models. Ultimately, the study provides a molecular framework for developing new therapeutic strategies against these aggressive and lethal childhood brain tumors.

References:

• Bernardi F, Torrejon J, Basili I, et al. Multiomic integration reveals tumoral heterogeneity of lipid dependence within lethal group 3 medulloblastoma[J]. Cancer Cell, 2026.