S820
Clinical - Lung
ESTRO 2026
(Figure 1).
TRT provides durable local control and favorable survival outcomes, with acceptable side effects. Keywords: radical thoracic re-irradiation, NSCLC patients
Digital Poster 3518 SIRPβ1 insertion exposes a prognostic immunogenomic vulnerability in small-cell lung cancer Elías Gomis Sellés 1 , Emilio Alarcon-Martin 2,3 , Manuel Borrego 4 , Gabriela Antelo 1 , María José Bravo 2 , José Luís Royo 2 , José Luís López Guerra 4 1 Radiation Oncology, Hospital Clínic, Barcelona, Spain. 2 Departamento de Especialidades Quirúrgicas, Bioquímica e Inmunología, Facultad de Medicina,, University of Malaga, Malaga, Spain. 3 Research Center and Memory Clinic, ACE Alzheimer Center Barcelona, Universitat Internacional de Catalunya, Barcelona, Spain. 4 Radiation Oncology, Hospital Universitario Virgen del Rocío, Sevilla, Spain Purpose/Objective: Lung cancer remains the leading cause of cancer- related mortality, with immune escape as a central driver of its relentless progression. The signal regulatory protein family has emerged as a critical immune checkpoint axis. Within this family, SIRP β 1 is unique: a structural Copy-Number Variant (CNV) introduces isoforms with distinct extracellular and transmembrane domains, reshaping DAP12-
In our cohort, SCLC patients harboring the rs2209313- T (insertion) allele showed a strikingly worse prognosis, with a nearly threefold increased risk of relapse (HR 2.806; 95% CI 1.098–7.170; p = 0.043) (figure 2). Median disease-free survival dropped to 6.0 months in carriers versus 10.1 months in non-carriers. The trend extended to local recurrence (p = 0.065), underscoring a consistent deleterious effect in this aggressive subtype. Importantly, no significant associations were found in NSCLC (p > 0.05), pointing to a histology-specific biological role of SIRP β 1.
dependent signaling. Material/Methods:
Conclusion: This is the first study to implicate the SIRP β 1 insertion allele as a driver of poor prognosis in small-cell lung cancer. By reshaping isoform diversity and SYK- mediated signaling, this CNV may fuel immune evasion and accelerate tumor progression. Our findings illuminate an uncharted immunogenomic axis in SCLC, raising the possibility that SIRP β 1 status could influence responses to immunotherapy and guide patient stratification. Keywords: SIRP β 1, inflammation, Copy-number variant Digital Poster 3593 Contralateral Hilar Irradiation in Lung Cancer: A Systematic Review Shigeo Takahashi 1 , Nobuki Imano 2 , Noriko Kishi 3 1 Department of Radiation Oncology, Kagawa University Hospital, Kagawa, Japan. 2 Department of Radiation Oncology, Hiroshima University Hospital, Hiroshima, Japan. 3 Department of Radiation Oncology
We hypothesized that this insertion modifies macrophage-driven inflammation, alters tumor– immune crosstalk, and impacts clinical outcomes. Our goal was to characterize its prognostic value in patients with lung cancer treated with radiotherapy.We retrospectively included 121 patients (88 NSCLC; 33 SCLC) treated with definitive radiotherapy. CNV genotype was inferred through rs2209313, in strong linkage disequilibrium with the insertion allele. Clinical and treatment variables were analyzed, and associations with recurrence and survival were tested. To strengthen biological plausibility, immunohistochemistry data from the Human Protein Atlas (n = 489) were interrogated for SIRP β 1 expression across lung cancer subtypes. Results: Genotype frequencies were consistent with Hardy– Weinberg equilibrium and with European population data, suggesting the CNV is not a risk factor per se.However, Protein Atlas analysis revealed that higher SIRP β 1 expression correlated with reduced disease- free survival in squamous cell carcinoma (57% vs. 42%, p = 0.042), an effect not observed in adenocarcinoma
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