ESTRO 2025 - Abstract Book

S421

Clinical - Biomarkers

ESTRO 2025

4496

Digital Poster The influence of radiotherapy on cellular senescence Katarzyna Paal 1 , Bettina Stranz 1 , Eva-Maria Thurner 1 , Wilfried Renner 2 , Tanja Langsenlehner 1 1 Radiooncology, Medical University of Graz, Graz, Austria. 2 Laboratory medicine, Medical University of Graz, Graz, Austria Purpose/Objective: Cellular senescence occurs throughout life and can be triggered by a variety of cell-intrinsic and extrinsic stimuli. Mean telomere length is one of the few indicators proposed to reliably identify senescent cells. Telomeres are protein-bound DNA repeat structures at the end of chromosomes which are protecting chromosomes from damage during each cell division and, thus, play a critical role in maintaining chromosomal stability. During somatic-cell replication, telomere length progressively shortens because of the inability of DNA polymerase to fully replicate the 3′ end of the DNA strand. Within an individual, mean leucocyte telomere length (LTL) and telomere length in other tissues are highly correlated, making the use of telomere length obtained from peripheral blood leucocytes a potential biomarker of aging. In the present study, we analyzed the influence of radiotherapy on leucocyte telomere length (LTL). Material/Methods: A total of 314 patients treated with curative radiotherapy for prostate cancer were included in the present prospective study. Measurement of LTL was performed at baseline (within 2 weeks prior to initiation of radiation therapy), at the end of radiotherapy as well as 3 and 15 months after completion of radiotherapy. After isolation of genomic DNA, LTL was assessed using relative telomere length (RTL)-qPCR . Results: The mean RTL values were 0.65 ± 0.34 kb at baseline, 0.62 ± 0.31 kb at the end of radiotherapy, 0.67 ± 0.43 kb, and 0.55 ± 0.26 kb at the first and at the second follow-up, respectively. Paired-Samples T-Test comparisons showed a significant decrease in RTL at second follow-up when compared to the baseline (p<0.001) and to the end of RT (p=0.001), as well as a significant decrease of RTL between the first and second follow-up (p<0.001). Conclusion: In our cohort, we observed a significant shortening of telomeres at the follow-up examinations 3 and 15 months after treatment when compared to the baseline suggesting a negative impact of ionizing radiation on telomere length. References: Allsopp RC, Vaziri H, Patterson C, et al. Telomere length predicts replicative capacity of human fibroblasts. Proc Natl Acad Sci USA 1992;89:10114–8. Slagboom PE, Droog S, Boomsma DI. Genetic determination of telomere size in humans: a twin study of three age groups. Am J Hum Genet 1994;55:876–82. Njajou OT, Cawthon RM, Damcott CM, et al. Telomere length is paternally inherited and is associated with parental lifespan. Proc Natl Acad Sci USA 2007;104:12135–9. Kordinas V, Ioannidis A, Chatzipanagiotou S. The telomere/telomerase system in chronic inflammatory diseases. Cause or effect [serial online]? Genes (Basel) 2016;7:E60. Keywords: aging, cellular senescence, telomere length