S2620
Radiobiology - Translational radiobiology
ESTRO 2026
Heidelberg University Hospital (UKHD), Heidelberg, Germany. 5 Medical Physics, Heidelberg Ion Beam Therapy Center (HIT), Heidelberg, Germany Purpose/Objective: We report at ESTRO the promising clinical phase II trial (PACK) results of Carbon ion radiotherapy (CIRT) in pancreatic ductal adenocarcinoma (PDAC). Moreover, translational studies (PACK/TRACK) indicate potential role for adaptive immunity underlying CIRT efficacy. Therefore, from a Bed-to-Bench side perspective, we sought to investigate the impact of adaptive immune response on CIRT induced tumor control probability (TCP). Material/Methods: KPCY-2838c3 tumor derived from LSL-KrasG12D/+;LSL- Trp53R172H/+;Pdx-1-Cre; YFP, KPCY genetically
engineered mouse model (GEMM) were subcutaneously implanted into syngeneic
immunocompetent C57BL/6. Mice were randomized when tumors reached 80 ± 30 mm ³ . Tumors were irradiated at the mid region of the spread-out Bragg peak (SOBP) with high linear energy transfer (LETd of 95 keV/µm). Dose escalation series was conducted at five consecutive daily fractions of 3, 4 and 5 Gy. To evaluate the impact of the adaptive T-cell response, all experiments were also conducted in immunocompromised nude mice. The impact of cytotoxic T-Cell response was further functionally validated using anti-CD8 (aCD8) depleting antibodies. Results: The TCP gradually increased from 27% at 5x3Gy to 83% after 5x5Gy. In contrast, TCP was not reached up to 5x5Gy in nude mice lacking anti-tumoral T-cell immunity. Moreover, depletion of cytotoxic T-cells by aCD8 substantially reduced CIRT induced therapeutic efficacy. Conclusion: High-LET CIRT efficiently eradicates otherwise therapy resistant KPC GEMM. Adaptive anti-tumoral T-cell response plays a pivotal role for achievement of tumor control governed by CIRT in PDAC. Keywords: Pancreatic Cancer, Ion Therapy, Immune System Digital Poster 3052 A blood leucocyte-based radiotherapy transcriptomic prognostic signature in prostate, cervical, and bladder cancer. Jeronimo Leberle 1 , Conrado Guerrero Quiles 2 , Taha Lodhi 2 , Laura Mazzitelli-Fuentes 3 , Lara Negrin 3 , Soledad Ausas 3 , Anubhav Datta 4,2 , Lisa Barraclough 4 , Kate Haslett 4 , Nicolas Bellora 1 , Irene L. Ibañez 5 , Kimberley Reeves 2 , Catharine M. West 2 , Peter Hoskin 4,6 , Ananya Choudhury 2,4 , Luisa V. Biolatti 2
Figure 2: pATM (A) and γ -H2AX (B) foci kinetics in normal and FA skin following drug pre-treatment and 2 Gy IR. p-values are represented as *p<0.05, **p<0.01, ***p<0.001 when comparing with 2 Gy alone. Conclusion: Our findings indicate thatFA fibroblasts display impaired DNA-DSB repair capacity and genomic instability. Moreover, ZoPra enhances DNA-DSB repair efficiency, ultimately improving post-irradiation survival without increasing genomic instability. These findings support ZoPra as a promising pharmacological strategy to mitigate radiosensitivity in FA. Keywords: Friedreich’s Ataxia, DNA repair, radiosensitivity Proffered Paper 2317 The Impact of Adaptive Immunity in Local Control of Pancreatic Cancer by Carbon Ion Therapy Saleh Eskandarian 1,2 , Mahmoud Moustafa 1,2 , Maximilian Knoll 1,2 , Mahdi Akbarpour 1,2 , Henry Meyer 3 , Aoife Gahlawat 1,2 , Felix Englert 4 , Stephan Brons 5 , Julian Schlegel 1,2 , Klaus Herfarth 4 , Jurgen Debus 1,2 , Jakob Liermann 4 , Amir Abdollahi 1,2 1 Clinical Cooperation Unit Translational Radiation Oncology, German Cancer Research Center (DKFZ), Heidelberg, Germany. 2 Molecular and Translational Radiation Oncology, Medical Faculty Heidelberg University (MFHD), Heidelberg, Germany. 3 Radiation Physics, University of Texas MD Anderson Cancer Center, Houston, TX, USA. 4 Radiation Oncology,
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