Abstract
Diffuse gliomas are the most frequent brain tumours, representing 75% of all primary malignant brain tumours in adults. Because of their locally aggressive behaviour and the fact that they cannot be cured by current therapies, they represent one of the most devastating cancers. The present review summarises recent advances in our understanding of glioma development and progression by use of various in vitro and in vivo models, as well as more complex techniques including cultures of 3D organoids and organotypic slices. We discuss the progress that has been made in understanding glioma heterogeneity, alteration in gene expression and DNA methylation, as well as advances in various in silico models. Lastly current treatment options and future clinical trials, which aim to improve early diagnosis and disease monitoring, are also discussed.
Highlights
A brain tumour is formed when there is an abnormal clonal growth of cells within the brain
To form neurospheres, freshly resected human glioma cells are grown in a serum-free medium containing basic fibroblast growth factor, epidermal growth factor (EGF), and the neuronal cell culture supplement B-27 [45,46,47]
By using single cell RNA-sequencing, they identify a subset of genes that were differentially expressed in patient samples that had been co-cultured with healthy organoids compared to patient samples with no co-culture or healthy organoids cultures alone. This gene set was upregulated across all GBM samples that had been co-cultured and included: Gap Junction Protein Alpha 1 (GJA1) encoding connexin-43, which allows gap junctions to form between GBM microtubes; Collagen Type IV Alpha 5 Chain (COL4A5) which encodes for a component of the extracellular matrix, and Glypican 3 (GPC3), an activator of the Wnt signaling pathway previously associated with invasiveness
Summary
A brain tumour is formed when there is an abnormal clonal growth of cells within the brain. A major achievement in the WHO classification of 2016 is the (subtotal) omission of the previously ill-defined diagnoses of oligoastrocytoma and anaplastic oligoastrocytoma By using both genotype (i.e., IDH mutations and 1p19q codeletion status) and phenotype as diagnostic criteria, most (if not all) tumours of this group fall into the category of oligodendroglioma or astrocytoma [33,34,35]. To the CNS WHO 2016 classification criteria, the oligoastrocytoma diagnosis needs to be used only when diagnostic molecular testing is not available, or in the rare real cases where a diagnosis based on histological and molecular genetic features has identified a mixed population of oligodendroglioma and astrocytoma cells within the tumours
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