ESTRO 2024 - Abstract Book

S5264 ESTRO 2024 anti-fibrotic effects by inhibiting NF-κB, mitogen-activated protein kinases (MAPKs), and Smad2/3 signaling pathways, both in vitro and in vivo. Radiobiology - Normal tissue radiobiology

Conclusion:

The synthetic LXA4 analogue offers the benefit of reducing damage during the early inflammatory phase, thereby preventing radiation-induced inflammation from progressing to fatal and irreversible pulmonary fibrosis. Our findings indicate that synthetic LXA4 analogue may be potential therapeutic candidate for minimizing radiation induced lung fibrosis and pneumonia.

Keywords: lipoxin A4, radiation, inflammation, NF-κB, Smad

1603

Digital Poster

Early cardiac functional and gene expression markers after irradiation of cardiac substructures

Cecilia Facchi 1 , Ardiansah Nugroho 2 , Duncan Forster 3 , Sukhpal Prehar 2 , Min Zi 2 , Sami Al-Othman 2 , Dandan Xing 2 , Hanan Abomanhal Masarweh 4 , Marilena Hadjidemetriou 4 , Mihaela Ghita 5 , Karl Butterworth 5 , Elizabeth Jane Cartwright 2 , Kaye Williams 6 1 The University of Manchester, Cancer, Manchester, United Kingdom. 2 The University of Manchester, Cardiovascular, Manchester, United Kingdom. 3 The University of Manchester, Informatics, Imaging & Data Sciences, Manchester, United Kingdom. 4 The University of Manchester, Cell Matrix Biology & Regenerative Medicine, Manchester, United Kingdom. 5 Queen's University Belfast, Cancer, Belfast, United Kingdom. 6 The University of Manchester, Pharmacy & Optometry, Manchester, United Kingdom The main purpose of this project is the identification of potential early functional markers for the detection of radiation-induced cardiac toxicity (RICT) and the prevention of later onset of severe cardiac phenotype. This would include both parameters from electrocardiogram (ECG), echocardiography, and mechanistic understanding through gene expression at the tissue level. Radiation therapy (RT) is extensively used in the treatment of cancer and is prescribed to over 50% of all cancer patients. Despite advancements in RT technology that aim to precisely target the tumor volume, healthy tissues are inevitably exposed to radiation. In patients undergoing RT for thoracic malignancies, this can result in RICT, wherein the heart is exposed to radiation and subsequently develops various pathologies, such as myocardial fibrosis and arrhythmias several years after treatment 1 . Recent clinical evidence has established a strong association between cardiovascular outcomes and specific substructures of the heart affected by RT, particularly when the base of the ventricle is the main affected area 2 . Numerous preclinical studies have investigated the potential pathophysiological mechanisms underlying RICT, emphasizing the importance of accurately defining the substructures impacted by radiation in order to determine the molecular mechanisms of RICT 3 . However, a comprehensive understanding of the molecular and functional changes occurring in cardiac tissue is still lacking, particularly in terms of identifying early markers that would enable proper monitoring of patients. Purpose/Objective: