Michelle M. Kushida

This study identifies SAT1 as a key driver of quiescence in glioblastoma stem cells through metabolic rewiring and viral mimicry, showing it can induce reversible growth arrest.

This study develops a mouse model of pediatric gliomas and identifies BRAF and MAPK signaling as critical drivers of tumor progression and therapeutic resistance.

The paper shows that glioblastoma stem cells form spatial patterns correlated with their transcriptional state, using image analysis to link morphology and gene expression.

This paper identifies PRMT5 as a regulator of HTT mRNA splicing and alternative polyadenylation, showing that its inhibition reduces full-length HTT protein levels by promoting premature termination and cleavage.

This study uses CRISPR-Cas9 screens in patient-derived glioblastoma stem cells to identify essential genes and pathways for stemness and drug resistance, revealing new therapeutic targets.