Abstract Book

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viability (A549 and NCL-H23) and tubule formation (HUVECs). At a cellular level the DNA damage response and alteration to cell cycle progression were assessed using both immunocytochemistry and flow cytometry techniques. Results The clonogenic survival in response to broad bream irradiation was fitted to the linear quadratic model. The resulting survival curve was then used to calculate a predicted response to the microbeam. This prediction assumed that 1/8 of cells received the peak dose, 7/8s the valley dose and that there was no communication between cells in the peaks and the valleys. The survival of both the tumour cell lines A549 and NCL- H23 fell below the predicted response, indicating that communication between the cell lines enhances the effectiveness of the microbeam. However, the survival of MRC-5 and HUVECs was as predicted or higher indicating a possible sparing effect as a result of communication between cells in the peaks and the valleys. Cell cycle analysis reveals stark differences in the cell cycle response to broad beam and microbeam radiations in tumour cell lines.

Conclusion This work proves the feasibility of the transfer of MBRT outside synchrotron sources towards a small animal irradiator. In addition, the gain in tissue resistance obtained with millimetre beams (968 ± 77 µm) is a valuable finding in the context of general indication in the literature that the minibeams’ tissue-sparing effect starts to rapidly decline above 0.7 mm beam thickness. This is the first time that such an evaluation is done with millimetre-sized minibeams in the brain. This result has important implications for potential clinical trials, since it opens the door for future implementations with less technically demanding and very compact systems and, even with modified Linear Medical Accelerators. [1] Prezado, Y. et al. Rad Research 184 , 314–21 (2015). [2] Prezado, Y. et al. Med. Phys. 38 , 5012–5020 (2011). PV-0568 Remarkable normal tissue sparing effects are seen in vitro in response to microbeam radiation. H. Steel 1 , C. Box 1 , U. Oelfke 1 , S. Bartzsch 1,2 1 Institiute of Cancer Research, Physics, London, United Kingdom 2 Technical University of Munich, Department of Radiation Oncology, Munich, Germany Purpose or Objective The damage to normal tissues remains a major concern of treating patients with radiotherapy and is often a limiting factor in the dose of radiation that is able to be administered to the tumour. Microbeam radiation therapy (MRT) has shown great promise in small animal models, where normal tissue is extraordinarily tolerant to microbeams even at peak dose of up to several 100 Gy. These same doses cause significant tumour growth delay and in some cases ablation. However the mechanism behind this differing response between normal and tumour tissues remains unknown. Whist in-vivo experiments provided manifold evidence for normal tissue sparing of MRT, there is little in vitro data that demonstrates the extraordinary normal tissue response . Our aim was to assess if the normal tissue tolerance to MRT remains in vitro and to understand the underlying mechanism on a cellular level. Material and Methods Microbeams were produced using a conventional x-ray tube and a bespoke collimator resulting in the production of 49 50µm wide beams each 400µm apart with a peak to valley dose ratio of 20. This setup has been dosimetrically validated previously and measured dose distributions are comparable to those generated at the European synchrotron. The effect of both broad beam and microbeam radiation was tested on both normal (MRC-5 and HUVECs) and tumour (A549 and NCL-H23) lung cells in vitro. Broad beam doses were compared to the integrated microbeam dose. The clonogenic survival of all cell lines was assessed as well as the effect on spheroid growth and

Conclusion Our data demonstrates that the stark differences between normal and tumour cell response to MRT can be seen in vitro . The differences recorded between the predicted microbeam survival and actual survival suggests that communication between cells plays a substantial role in the microbeam response. PV-0569 Proton minibeam radiation therapy widens the therapeutic window for gliomas Y. Prezado 1 , W. Gonzalez 1 , A. Patriarca 2 , G. Jouvion 3 , C. Nauraye 2 , C. Guardiola 1 , D. Labiod 4 , M. Juchaux 1 , L. Jourdain 5 , C. Sebrie 5 , F. Pouzoulet 4 1 Centre National de la Recherche Scientifique, Imagerie et Modélisation en Neurobiologie et Cancérologie, Orsay, France 2 Institut Curie, Orsay Proton Therapy Center, Orsay, France 3 Institut Pasteur, Anatomopathology and Animal models, paris, France 4 Institut Curie, Experimental Radiotherapy Platform, Orsay, France 5 University Paris Sud, IR4M, Orsay, France Purpose or Objective The morbidity of normal tissues continues being the main limitation in radiotherapy. To overcome it, we proposed a novel concept: proton minibeam radiation therapy (pMBRT) [1]. It allies the physical advantages of protons with the normal tissue preservation observed when irradiated with submillimetric spatially fractionated beams (minibeam radiation therapy) [2]. We have recently implemented this technique [3] at a clinical center (Proton therapy center in Orsay) and