ESTRO 36 Abstract Book

S850 ESTRO 36 2017 _______________________________________________________________________________________________

All plans for all patients reached prescription doses while adhering to dose constraints. The average volumes of GTV- histo, GTV-union and GTV-intersection were 7±8 ml, 9±9 ml and 3±4 ml. In Plan95 union and Plan95 intersection the mean doses on GTV-histo were 95.7±1.5 Gy and 90.7±6.9 Gy, respectively (p=0.016). Average TCP-histo values were 63±29%, 99±1% and 90±11% for Plan77, Plan95 union and Plan95 intersection respectively. PLAN95 union had significantly higher TCP-histo values than Plan77 (p=0.016) and Plan95 intersection (p=0.03). There were no significant differences in rectal and bladder NTCPs between the 3 plans. Conclusion IMRT dose painting for primary PCa using combined 68 Ga- HBED-CC PSMA-PET/CT and mpMRI was technically feasible. A dose escalation to GTV-union resulted in significantly higher TCPs without higher NTCPs. V. Aubert 1,2 , O. Acosta 1,2 , N. Rioux-Leclercq 3 , R. Mathieu 4 , F. Commandeur 1,2 , R. De Crevoisier 1,2,5 1 INSERM, U1099, Rennes, France 2 University Rennes 1, LTSI, Rennes, France 3 Rennes Hospital and University, Department of Pathology, Rennes, France 4 CHU Pontchaillou, Department of Urology, Rennes, France 5 Centre Eugène Marquis, Department of Radiotherapy, Rennes, France Purpose or Objective Using simulation from histopathological cancer prostate specimen, the objectives were to identify the total dose corresponding to various fractionations necessary to destroy the tumor cells (50% to 99.9%) and to assess the impact of the Gleason score on these doses. Material and Methods Histopatological specimen were extracted from 7 patients having radical prostatectomy. A senior uropathologist manually delineated all tumor foci on the hematoxylin and eosin-stained axial slides and assigned Gleason scores (GS) to each individual focus. Antibodies CD31 were used as blood vessel markers. Three slide samples per patient, corresponding to a surface of 2000µm x1200µm, were scanned and used within a simulation model developed in the Netlogo software (Figure 1). The model contained the following cells: tumor cells with a density ranging from 45% to 85%, endothelial cells with a density ranging from 0.3 to 8% and normal cells. The samples were GS:7 (3+4) for 47.6%, GS:7 (4+3) for 28.6% and GS:8 (4+4) for 23.8%. We used the equations of the model simulating the radiation response of hypoxic tumors published by Espinoza et al. (Med Phys 2015) . The model parameters were adjusted to biological values from the literature: diffusion coefficient (2.10 -9 m²/s), Vmax and Km of oxygen consumption (15 and 2.5 mmHg), tumor cells proliferation (1008 hours), half-life of dead cells (168 hours), α (0.15 Gy -1 ) and β (0.048 Gy -2 ) of the linear-quadratic model. Three fractionations were tested, at 2, 2.5 and 3 Gy/fraction at 24h interval. Five simulations were performed by slide sample. The objectives were to identify the total dose, at each fractionation, to kill 50% to 99.9% of the tumor cells. EP-1598 Modelisation of radiation response at various fractionation from histopathological prostate tumors

Results A total of 315 simulations were performed. Figure 2 shows the total doses necessary to kill 50% to 99.9% of the tumor cells, depending on the fractionation. The mean (SD) doses (Gy) to kill 99% of the tumor cells were therefore 72 (±14), 68 (±13) and 65 (±12) for fractionations (Gy) of 2, 2.5 and 3, respectively. The mean (SD) doses (Gy) to kill 99.9% of the tumor cells were therefore 107 (±17), 101(±16) and 94 (±15) for fractionations (Gy) of 2, 2.5 and 3, respectively. The foci with GS 7: 4+3 needed significantly higher doses than the foci with GS 7: 3+4 to destroy the tumor cells from 50% to 99.9%, at all fractionations (Mann-Whitney test).

Conclusion Our histopathological specimen based simulations allowed to estimate the total doses necessary to kill the tumor cells, depending on the fractionation. GS: 4+3 tissue appears more radioresistant than GS:3+4 tissue. EP-1599 Mathematical modeling of the synergistic combination of cancer immunotherapy and radiotherapy C. Ceberg 1 , J. Ahlstedt 2 , H. Redebrant Nittby 3 1 Ceberg Crister, Medical Radiation Physic- Lund University, Lund, Sweden 2 Lund University, The Rausing Laboratory, Lund, Sweden 3 Skåne University Hospital, Department of Neurosurgery, Lund, Sweden Purpose or Objective Cancer immunotherapy is a promising treatment modality that is currently under strong development with a large number of ongoing pre-clinical and clinical studies. In an attempt to improve the treatment efficacy combinatorial strategies are explored, and the combination of immunotherapy and radiotherapy is of particular interest, since more than half of all cancer patients already receive radiotherapy as part of their treatment. It is well known that radiation has immunomodulatory effects. In addition to killing off tumor cells as well as immune effector cells, radiation also affects the release of tumor antigens, the dendritic cell activity and antigen presentation, the