S2586
Radiobiology – Normal tissue radiobiology
ESTRO 2026
Turkey. 5 Experimental Animals Laboratory, Koç University Research Center for Translational Medicine (KUTTAM), Istanbul, Turkey. 6 Radiation Oncology, American Hospital, Istanbul, Turkey Purpose/Objective: Radiation-induced lung injury (RILI) remains a major dose-limiting side effect in thoracic radiotherapy. In its acute phase, it presents as radiation pneumonitis, typically managed with corticosteroids. However, corticosteroid use carries notable drawbacks, including reduced efficacy of concurrent immune checkpoint inhibitors, limited prevention of late-stage pulmonary fibrosis, and significant adverse effects with prolonged administration. Given the central role of cytokines in RILI pathogenesis, this study aimed to evaluate the therapeutic efficacy of tocilizumab, an interleukin-6 (IL-6) receptor antibody, in a preclinical
Conclusion: Administration of an anti-IL-6 receptor antibody mitigated radiation-induced pulmonary injury in mice, albeit without statistical significance, and notably reduced radiation-induced skin reactions. These findings suggest a potential radioprotective role for IL- 6 blockade. Further clinical studies evaluating tocilizumab for the prevention or management of radiation-induced toxicities—particularly in breast and head-and-neck cancer patients—merit exploration. References: Rube CE, Uthe D, Wilfert F, et al. The bronchiolar epithelium as a prominent source of pro-inflammatory cytokines after lung irradiation. Int. J. Radiat. Oncol. Biol. Phys. 2005;61(5):1482-92.Arpin D, Perol D, Blay JY, et al. Early variations of circulating interleukin-6 and interleukin-10 levels during thoracic radiotherapy are predictive for radiation pneumonitis. J. Clin. Oncol. 2005;23(34):8748-56. Keywords: Radiation pneumonia, fibrosis, interleukin- 6 Early adipocyte lipolysis in dermal white adipose tissue precedes and initiates radiation dermatitis Shih-fan Lai Radiation oncology, National Taiwan university cancer center, Taipei, Taiwan. Oncology, National Taiwan university hospital, Taipei, Taiwan Purpose/Objective: Given that lipid metabolism underpins skin barrier and immune homeostasis yet mechanisms of radiation dermatitis (RD) remain unclear, we tested whether radiation-induced alterations in adipocyte lipid metabolism within dermal white adipose tissue (dWAT) precede and initiate RD, providing quantitative mechanistic evidence to guide prevention. Material/Methods: Digital Poster 4824 C57BL/6 mice underwent localized single-fraction 40 Gydorsal irradiation. RD was graded longitudinally by blinded assessors, and skin was analysed by H&E and immunofluorescence with compartment-resolved morphometrics (adipocyte droplet area, tissue thickness). Quantification was performed under blinding and evaluated using appropriate statistical
murine model of RILI. Material/Methods:
Forty C57BL/6 mice were included in the study. A single fraction of 20 Gy ionizing radiation (IR) was delivered to the upper lobe of the right lung. Anti- mouse IL-6 receptor antibody (IL-6RA) was administered intraperitoneally on days 1, 4, and 7 post-irradiation. Five mice per group were randomly sacrificed on day 70 to assess early-phase findings, while the remainder were sacrificed on day 150 for late-phase evaluation. Lung and skin tissues were examined histopathologically. Clinical and dermatologic observations were recorded throughout the study. Results: Mice receiving radiation alone developed significantly higher grades of radiation dermatitis (RTOG criteria) compared with those treated with the IL-6 receptor antibody (p = 0.005). Although histopathologic total lung injury scores—evaluating alveolar, peribronchiolar, perivascular, and interstitial regions— were higher in the radiation-only group, the difference did not reach statistical significance (Figure 1). Dermal fibrosis was significantly more pronounced in the radiation-only group versus the antibody-treated group (Figure 2) (p = 0.006).
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