S2547
Radiobiology - Microenvironment
ESTRO 2026
Digital Poster Highlight 2215 Immune Effects of Neoadjuvant Chemotherapy on Muscle Invasive Bladder Cancer Amen Shamim 1,2 , Mark Reardon 1 , Vanesa Luisa Biolatti 1 , Conrado Guerrero Quiles 1 , Jamie Honeychurch 1,3 , Eleanor J Cheadle 3 , Pedro Oliveira 4 , Vodathi Bamunuarachchi 5 , Kimberly Reeves 1 , Peter Hoskin 1,6 , Richard Walshaw 7 , Ananya Choudhury 1,5 1 Translational Radiobiology Group, Division of Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine & Health, University of Manchester, Manchester, United Kingdom. 2 Department of Computer Science, University of Agriculture, Faisalabad, Pakistan. 3 Targeted Therapy Group, Division of Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine & Health, University of Manchester, Manchester, United Kingdom. 4 Department of Pathology, The Christie NHS Foundation Trust, Manchester, United Kingdom. 5 Department of Clinical Oncology, The Christie NHS Foundation Trust, Manchester, United Kingdom. 6 Mount Vernon Cancer Centre, Mount Vernon Hospital, Northwood, United Kingdom. 7 The Clatterbridge Cancer Centre, NHS Foundation Trust, Manchester, United Kingdom Purpose/Objective: Patients with non-metastatic muscle-invasive bladder cancer (nmMIBC) are treated with either radical cystectomy or organ-sparing chemoradiotherapy (CRT) with similar survival outcomes. Cisplatin-based neo- adjuvant chemotherapy (NAC) is standard-of-care before definitive treatment. nmMIBC patients whose tumours have high levels of immune infiltration have better survival outcomes after CRT1,2,3. Although NAC can enhance immune infiltration in some cancers and hypoxia is also associated with increased immune infiltration4, the effects of NAC on the tumour microenvironment (TME) in nmMIBC have not been fully explored. We hypothesised that NAC increases immune infiltration in nmMIBC. Material/Methods: Patients with MIBC (n = 57) treated between 2008 and 2022 were identified with confirmed muscle infiltration on diagnostic biopsy or imaging. FFPE diagnostic biopsies were collected before and after treatment. Whole RNA was extracted and sequenced with Illumina-Novaseq (Figure 1).
Conclusion: Dietary I3C emerges as a candidate therapy for radiation proctitis by restraining MMT, thereby reducing epithelial injury and fibrosis in RP. References: 1. Andreyev, H.J., GI Consequences of Cancer Treatment: A Clinical Perspective. Radiat Res, 2016.2. Grodsky, M.B. and S.M. Sidani, Radiation proctopathy. Clin Colon Rectal Surg, 2015. 3. Hayne, D., C.J. Vaizey, and P.B. Boulos, Anorectal injury following pelvic radiotherapy. Br J Surg, 2001. 88(8)4. Lu, W., et al., Platelet-derived growth factor C signaling is a potential therapeutic target for radiation proctopathy. Sci Transl Med, 2021. 5. Chen, J., et al., P2Y12 inhibitor clopidogrel inhibits renal fibrosis by blocking macrophage-to-myofibroblast transition. Mol Ther, 2022. 6. Wang, Y.Y., et al., Macrophage-to- Myofibroblast Transition Contributes to Interstitial Fibrosis in Chronic Renal Allograft Injury. J Am Soc Nephrol, 2017. Keywords: radiation proctitis, indole-3-carbinol
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