English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Malignant glioma can be understood as a cancer stem cell disease. There is strong evidence that expression of a core set of neural stem cell master regulators is necessary and sufficient for tumour initiation in both adult and childhood disease subtypes, and across a range of underlying mutation signatures and expression profiles. We hypothesise that a double positive SOX2+ OLIG2+ progenitor is the cancer stem cell in H3K27M diffuse intrinsic pontine glioma (DIPG) and adult glioblastoma (GBM) alike. We present expression data in 4 patient-derived cell lines (2 adult GBM, 2 DIPG) in vitro and in a defined mutation mouse model of the H3K27M disease, demonstrating high expression levels of SOX2 and OLIG2 in serum-free culture and especially in the invasive tumour. We then demonstrate derivation of patient-derived human dual reporter lines, using a CRISPR targeting approach to add fluorescent reporters at the endogenous SOX2 and OLIG2 loci. With these tools, we aim to characterise the tumour-initiating potential of the SOX2+ OLIG2+ fraction. We further aim to identify cell surface markers whose expression is driven by this transcription program and which might represent targets for novel molecular therapies.

Characterising a SOX2+ OLIG2+ glioma stem cell using Crispr-engineered fluorescent reporters in primary patient-derived GBM and DIPG cells.