S3032
Invited Speaker
ESTRO 2026
environment for tumor growth. In addition, senescent stromal fibroblasts have an altered expression of several proteoglycans. They overexpress both in vitro and in vivo the Syndecan 1 (SDC1), a poor prognostic indicator for the disease progression. This is the effect of the autocrine action of Transforming Growth Factor - β (TGF - β ) through the Smad pathway and the transcription factor Sp1, while invasive cancer cells enhance SDC1 expression, via the paracrine action of TGF- β 1. In addition, they down regulate the expression of decorin, a change also considered a poor prognostic factor for breast cancer progression; this change is again mediated through the autocrine action of several growth factors (mainly FGF and VEGF). In addition, in different contexts it has been shown that senescent cells can deposit a senescence-promoting matrix and even induce metabolic changes in cancer cells, enhancing tumor development. The above indicate that senescent cells provoke a specific remodeling of their microenvironment, supporting tumor growth. 5417 Survey research that matters: ESTRO guidance for better design Amanda Webster Radiotherapy and PBT, UCLH, London, United Kingdom. Medical Physics & Biomedical Engineering, UCL, London, United Kingdom Survey-based research is increasingly used within radiation oncology to explore practice variation, inform guideline development, and capture professional perspectives across international settings. However, it is often undertaken without structured methodological guidance, leading to variability in quality and reporting. This session aims to provide a practical framework for designing, conducting, and reporting survey-based research in radiation oncology, designed for RO professionals who plan to undertake this type of work. This session is based on recently published guidance outlining key stages of the survey research pathway, including defining research questions, questionnaire development, piloting and validation, sampling strategies, survey distribution, and data analysis. Practical considerations such as minimising bias, ensuring content validity, optimising response rates, and aligning survey design with study objectives are addressed, supported by examples from radiation oncology practice. The guidance provides a structured approach to survey design and implementation, emphasising clarity in research objectives, robust questionnaire construction, and appropriate statistical handling of survey data. Common limitations in existing survey-
endothelial senescence from that observed in epithelial or stromal compartments. Finally, I will discuss how senescent endothelial cells reshape the vascular microenvironment through SASP-mediated crosstalk with neighboring fibroblasts, immune cells, and pericytes. Emerging evidence suggests that this senescence-driven vascular dysfunction may contribute to fibrosis development after radiation therapy. Collectively, these findings open new therapeutic avenues targeting senescent endothelial cells (e.g. through senolytics or senomorphics) to mitigate radiation-induced pulmonary fibrosis and improve long-term outcomes for thoracic radiotherapy patients.
5416 Ionising radiation-induced stromal fibroblast
senescence and tumor growth Eleni Mavrogonatou, Adamantia Papadopoulou, Manos Varveris, Harris Pratsinis, Dimitris Kletsas
Laboratory of Cell Proliferation and Ageing, Institute of Biosciences and Applications, NCSR "Demokritos", Athens, Greece While research on cancer development is traditionally focusing mainly on the neoplastic cell per se, nowadays the role of tumor stroma in this process is indisputable. With advancing age, the stroma exhibits alterations, important being the accumulation of senescent cells. Senescence can be triggered by exogenous stresses, including genotoxic anticancer treatment modalities (such as chemotherapy or radiotherapy) and is manifested as an inhibition of cell proliferation, ascribing to cellular senescence the role of a potent antitumor barrier. On the other hand, senescent cells, through their specific senescence- associated secretory phenotype (SASP) - comprising cytokines, growth factors, extracellular matrix (ECM) components and ECM-degrading enzymes - can establish an inflammatory and catabolic microenvironment that may stimulate tumor growth and metastasis. We have shown in in vitro experiments that non-cytotoxic, curative doses of ionizing radiation (IR) can promote premature senescence in stromal fibroblasts from various tissues (e.g. lung, breast, skin), although a subset of these cells can resist premature senescence. Interestingly, we have found also in vivo, in irradiated tissues in the framework of an anticancer treatment, the presence of a significant number of senescent cells. In addition, in xenograft mouse models, IR-mediated senescent stromal fibroblasts considerably increased the growth of cancer cells of different tissue origin. This growth was partly ascribed to the senescence-secreted matrix metalloproteases, which can create a permissive
Made with FlippingBook - Share PDF online