Poster #081
MacroH2A Modulates Glioblastoma Transcription
Mentor: Laurence Haddadin, Graduate Student
Glioblastoma is the most aggressive form of primary brain tumor, with around 14,000–15,000 new cases in the U.S. each year. The average survival time after diagnosis is 12–15 months, and only about 5–7% of patients live for five years. Despite decades of research, treatment outcomes have seen little improvement, underscoring a desperate need for new therapeutics. Recent studies suggest that epigenetic mechanisms, particularly those involving histone variants, might offer new ways to disrupt gene expression patterns that sustain glioblastoma stem cells (GSCs), a major factor in tumor recurrence and treatment resistance.
This project investigates whether the macroH2A histone variants play a role in modulating glioblastoma stemness. Preliminary data suggest that the macroH2As are involved in cell cycle regulation, and that overexpression (OE) alters cell phenotype. Specifically, OE may induce cell cycle arrest, suggesting a potential mechanism for reducing GSC (Glioblastoma Stem Cells) proliferation. These findings highlight the possibility of targeting the macroH2As and related epigenetic regulators as therapeutic strategies against glioblastoma.