ArticleMolecular cancer therapeutics2026
Immune Stromal Components Impede Biological Effectiveness of Carbon Ion Therapy in a Preclinical Model of Pancreatic Ductal Adenocarcinoma.
Article in Molecular cancer therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Challenges and opportunities in combining radiotherapy and immunotherapy for localized pancreatic cancer.Nature reviews. Gastroenterology & hepatology · 2026Review
- The link between macrophage polarization and response to radiotherapy in cancers: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Cryoablation Plus Immune Checkpoint Inhibitors Enhanced Dendritic Cell and T Cell Activation in TNBC Murine Model.ImmunoTargets and therapy · 2026Article
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12 authors.
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Abstract
The tumor landscape of pancreatic ductal adenocarcinoma (PDAC) is refractory to conventional photon radiotherapy (RT) because of a fibrotic tumor microenvironment (TME) that promotes chronic hypoxia and reduced immune surveillance. The radiobiological factors unique to carbon ion RT (CIRT), such as high linear energy transfer and less dependence on oxygen, make it well-suited to overcome the PDAC TME. In this study, we utilized clonal syngeneic KPC pancreatic tumor cell lines and tumors to examine this postulate and to identify underlying factors that affect the response of PDAC to CIRT. Although KPC cell lines exhibited radiobiological effectiveness greater than 3, subcutaneous tumors in the mouse hind leg showed lower radiobiological effectiveness-1.3 based on quintupling time-at a linear energy transfer between 70 and 80 keV/μm. Four days after CIRT, we observed widespread transcriptomic changes in the tumor immune microenvironment, suggesting increased infiltration of antitumor immune cells and elevated expression of antitumor T-cell cytokines, MHC class I molecules, and co-stimulatory signals. Fewer immunologic changes were observed following photon irradiation. By 7 days after CIRT, tumor-supportive transcriptomic programs characterized by protumor cytokines, M2 macrophages, and cancer-associated fibroblasts emerged, promoting resistance and limiting the durability of tumor growth delay. These findings suggest that CIRT may offer a favorable platform compared with conventional photon RT for combining with immunotherapies. Furthermore, these data highlight the risk of using in vitro survival data alone in treatment planning and indicate that underlying TME factors affect the response of PDAC in vivo.
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Registered trials
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