Friday, 08 October, 13:00
Presenter Professor Kevin Prise, Queen’s University Belfast, Topic: New Advances in Proton Therapy and the Underpinning Radiobiology
Kevin Prise is Professor of Radiation Biology, at the Patrick G Johnston Centre for Cancer Research, Queen’s University Belfast. He has developed wide-ranging interests in radiation biology including research on low dose radiation risk, radiation quality, cell and tissue signalling mechanisms. His recent work, at Queen’s has involved the development of an Advanced Radiotherapy Group (ARG) integrating Radiation Oncology and Clinical Radiotherapy Physics with Translational Radiation Biology. Together they are developing new biological based models for optimising advanced radiotherapies such as Intensity Modulated Radiotherapy, molecular radiotherapies and particle therapies. A current focus is on the development of new technologies for the precision delivery of particle therapies and optimization based on biologically driven relative biological effectiveness models.
Prof Prise received his PhD in Cell Biology and Biochemistry, from the University of Aberdeen, on the mechanisms of action of the chemotherapeutic methotrexate. He joined the Gray Laboratory, in Northwood London, in 1985 where he went on to become Head of the Cell and Molecular Radiation Biology Group. In 2007, he was recruited by Paddy Johnston to join the new Cancer Research Centre at Queen’s University Belfast
Proton therapy is increasingly being used as a cancer treatment, particularly for paediatric and difficult to treat tumours. The physical characteristics of proton beams with the delivery of a Bragg peak gives favourable conditions for delivery of radiation dose close to critical structures. There is also increased physical dose at depth, which has biological consequences. Specifically, more complex DNA damage is produced which is difficult for cells to repair. Our work has mapped this relationship between proton energy and DNA damage and survival response showing that protons can be greater than 2 times more effective at the end of their range in tissue. This more complex damage also requires different double-strand break repair pathways and more recent evidence suggests combinations of protons with DNA repair inhibitors may cause additional sensitisation in different patient subgroups.
Increasingly the impact of dose-rate on radiation response is becoming important. Recent studies with electrons delivered at “FLASH” dose-rates (> 40 Gy/s) have shown increased protection in normal tissues relative to tumour response. The mechanisms underpinning this are unclear, but may be related to the role of oxygen, a well-known sensitiser of radiation response and processing of reactive oxygen species. The impact of FLASH dose-rates is now being tested with proton therapy and if effective has the potential to accelerate the use of particle therapy in the future.