CRUK RadNet City of London Seminar Series

Chaired by Dr Simon Boulton, Group Leader at the Crick and Radiation Resistance Theme Lead, this seminar features talks from two of City of London's newest Postdocs.

10:30AM - 11:00AM (25min talk; 5min Q&A)

Jamie Dean - UCL Medical Physics and Biomedical Engineering and UCL Cancer Institute
Introducing the Computational Radiation Biology and Oncology Lab

Whilst radiotherapy is an effective treatment for numerous cancer patients, for many others it fails to control their tumours. Additionally, treatment often causes debilitating side effects. Increasing the success rate of radiotherapy requires understanding and manipulating the temporal evolution of tumours and normal tissues in response to treatment. In this talk I will introduce the goals and methods of the Computational Radiation Biology and Oncology Lab. We seek to quantitatively understand the dynamic responses of tumours and normal tissues to radiation and drug-radiation combination therapies. Exploiting this knowledge will enable us to design and evaluate novel treatment strategies to improve patient outcomes. We will achieve these aims through a multidisciplinary, collaborative approach, integrating mathematical and statistical modelling of molecular and cellular radiation response dynamics with longitudinal imaging and biological measurements of the response of cells, mice and patients to treatment.

11:00AM - 11:30AM (25min talk; 5min Q&A)

Lucy Brooks UCL Medical Physics and Biomedical Engineering and UCL Cancer Institute
The white matter is a pro-differentiative microenvironment for glioblastoma

Glioblastomas are hierarchically organised tumours driven by glioma stem cells that retain partial differentiation potential. Glioma stem cells are maintained in specialised microenvironments, but how they undergo lineage progression outside of these niches remains unclear. We have identified the white matter as a differentiative niche for glioblastoma. Tumour cells in contact with white matter acquire a pre-oligodendrocyte-like fate, resulting in decreased proliferation and invasion. Exploiting this latent programme may offer treatment opportunities for a subset of patients and has implications for radiation therapy.

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