Thibaut Barnoud

Abstract While outcomes for most children with medulloblastoma (MB) are relatively favorable, those in the Sonic Hedgehog (SHH) subgroup with Tumor protein P53 (TP53) mutations—known as the SHHα subtype—face a much poorer prognosis. SHHα patients relapse more frequently and rapidly, underscoring the need for therapies that prevent recurrence. We recently identified a non-canonical Gli-driven Sox2⁺ cell population that promotes relapse in SHH MB.

1 Introduction Inherited metabolic disorders can be caused by mutations of genes involved in the biogenesis, assembly or activity of metabolic enzymes, which can lead to enzymatic deficiency and severe life-threatening metabolic impairments (1). Metabolism is the process by which macromolecules (lipids, carbohydrates, nucleic acids, and proteins) are broken down to produce energy (catabolism) or used for energy storage (anabolism).

Carla Iacobini, Martina Vitale, Giuseppe Pugliese and Stefano Menini* Department of Clinical and Molecular Medicine, “La Sapienza” University, Rome, Italy The hypoxia-inducible factor-1α (HIF-1α), a key player in the adaptive regulation of energy metabolism, and the M2 isoform of the glycolytic enzyme pyruvate kinase (PKM2), a critical regulator of glucose consumption, are the main drivers of the metabolic rewiring in cancer cells.