Danielle Marsh was inspired to pursue further research into brain tumours during completion of an MSc in Biomedical Science, when she was involved in the development of advanced models for the study of tumours such as glioblastoma. The award of a Brain Research UK PhD studentship enabled her to pursue this ambition.
During her PhD, Danielle focused on the role of a protein called CBX2 in glioblastoma, and found evidence that targeting CBX2 triggers glioblastoma cell death and causes changes to glioblastoma cells that could make them more sensitive to existing treatments such as radiotherapy and chemotherapy.
Danielle was awarded her PhD in June 2026, and is now a postdoctoral researcher.
Glioblastoma is the most common primary brain cancer in adults, with around 2,500 cases diagnosed every year in the UK.
Glioblastoma is a grade 4 tumour, meaning that it grows and spreads quickly. It infiltrates the brain, wrapping finger-like tentacles around vital brain structures, making complete surgical removal impossible.
The current treatment strategy includes surgery to remove as much tumour as possible, followed by radiotherapy and chemotherapy to destroy remaining tumour. This prolongs survival but is not curative. Only a quarter of patients survive more than a year from diagnosis.
The need for new treatments is urgent.
Read more: About brain tumours
Epigenetics is a biological process that controls the way our genes behave by turning them on and off. In healthy cells, epigenetics is tightly controlled. In cancerous cells, however, the epigenetic control is faulty and can lead to uncontrolled cell growth. For her PhD, Danielle studied a protein called CBX2, which is known to be involved in epigenetic control, and which is found at higher levels in glioblastoma than in healthy brain tissue. CBX2 has been shown to have a role in other cancers, but has not been studied extensively in glioblastoma.
Danielle’s aim was to determine whether CBX2 is necessary for glioblastoma growth and whether it could therefore be a therapeutic target, through which tumour cell growth could be brought under control.
To do this, glioblastoma cells were treated with a specific compound (called SW2_152F), which blocks CBX2 from binding to DNA and carrying out its normal function. The effects of CBX2 inhibition on tumour cell growth, survival, and gene activity were then examined.
Danielle’s study showed that blocking CBX2 from binding to DNA reduced glioblastoma cell growth and triggered cell death. Further analysis indicated that CBX2 also regulates genes involved in the ‘cell cycle’, the process through which cells copy their DNA and divide to produce new cells. Inhibiting CBX2 caused tumour cells to accumulate DNA damage and allowed them to continue dividing before this damage could be repaired. This appeared to force the tumour cells into a fatal process known as ‘mitotic catastrophe’, whereby cell death is triggered through defective cell division.
Importantly, the study also assessed the effects of targeting CBX2 in living glioblastoma tumour tissue from patient donors, which was maintained in the laboratory using a specialised ‘chip’ device developed at the University of Hull. This chip allowed Danielle and her colleagues to closely monitor how glioblastoma tumour tissue reacts to different treatments. Encouragingly, targeting CBX2 in patient tissue produced similar anti-tumour effects to those observed in the glioblastoma cell models, strengthening the confidence that CBX2 is a clinically relevant target.
Danielle’s findings provide important new insight into the biological role of CBX2 in glioblastoma. The results suggest that CBX2 helps tumour cells survive DNA damage and continue proliferating, which raises the possibility that targeting CBX2 could make glioblastoma cells more sensitive to existing treatments such as radiotherapy and chemotherapy. Combining CBX2-targeted therapies with current standard treatments may therefore offer a new strategy for improving treatment effectiveness.
In the longer term, further development of CBX2-targeted therapies could contribute to more effective treatments for patients with glioblastoma, addressing a major unmet clinical need.
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