Abstract:In solid tumors, G0-like cell populations likely play important roles in maintaining cellular heterogeneity and promoting recurrence after standard of care. However, little is known about the mechanisms of tumor cell G0 ingress and egress. To discover regulators of G0-like states for glioblastoma (GBM), we performed a genome-wide CRISPR-Cas9 screen in patient-derived GBM stem-like cells (GSCs) for genes that trap cells in G0-like states when inhibited. We identify the protein acetyltransferase KAT5 as a key re… Show more
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