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Abstract
<p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" id="d1297349e77">Glioblastoma
(GBM) remains the most lethal primary brain cancer largely due to recurrence
of treatment-resistant disease. Current therapies are ultimately ineffective as GBM
tumour cells adapt their identity to escape treatment. Recent advances in single-cell
epigenetics and transcriptomics highlight heterogeneous cell populations in GBM tumours
originating from unique cancerous genetic aberrations. However, they also suggest
that tumour cells conserve molecular properties of parent neuronal cells, with their
permissive epigenetic profiles enabling them to morph along a finite number of reprogramming
routes to evade treatment. Here, we review the known tumourigenic, neurodevelopmental
and brain-injury boundaries of GBM plasticity, and propose that effective treatment
of GBM requires the addition of therapeutics that restrain GBM plasticity.
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