ArticleTechnology in cancer research & treatment
Combining Radiation and anti-PD-L1 Enhances the Antitumor Activity in Colorectal Cancer via IFN-γ-Dependent Activation of STAT1.
Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Primary and acquired resistance to immunotherapy in NSCLC.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
IntroductionColorectal cancer (CRC) remains a leading cause of cancer-related mortality, and proficient mismatch-repair/microsatellite-stable (pMMR/MSS) tumors respond poorly to immune checkpoint inhibitors (ICIs). Ionizing radiation (IR) can convert 'cold' tumors into 'hot' lesions but rarely elicits durable immunity alone.MethodsThis study investigated the synergistic antitumor effects of hypofractionated ionizing radiation (IR) combined with anti-PD-L1 therapy in CRC. Transcriptomic analysis of paired CRC biopsies (GSE179351) was performed to identify gene expression changes following combination therapy. In vivo efficacy was assessed in syngeneic BALB/c mice bearing CT26.WT tumors treated with 18 Gy IR (in 3 fractions) and anti-PD-L1 (10 mg/kg). Immunohistochemistry, flow cytometry, cytokine quantification, and Western blotting were used to evaluate immune cell infiltration, IFN-γ expression, and activation of JAK1/STAT1 signaling and apoptosis. To directly test the requirement of STAT1 signaling, CT26.WT cells were treated with the JAK1 inhibitor Itacitinib.ResultsCombination therapy induced 701 differentially expressed genes enriched in JAK-STAT signaling and apoptosis pathways. In vivo, IR + anti-PD-L1 significantly delayed tumor growth versus monotherapy without added systemic toxicity. Enhanced CD8
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