ArticleJournal of radiation research2025
Ultra-high dose rate (FLASH) carbon ion irradiation inhibited immune suppressive protein expression on Pan02 cell line.
Article in Journal of radiation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- For ultra-high dose rate carbon-ion irradiation, comparable beam parameters induce the equivalent cell sparing (FLASH) effect.Journal of radiation research · 2026Article
- Combined carbon ion radiotherapy and immunotherapy: leveraging the immunological advantages of carbon ion.Frontiers in immunology · 2026Review
- The potential and risks of FLASH radiotherapy in pediatric patients.Neuro-oncology pediatrics · 2026Review
- FLASH radiotherapy as an emerging paradigm in radioimmunotherapy: biological rationale, preclinical evidence, and translational roadmap.Frontiers in immunology · 2026Review
- Review
- Factors Influencing the Biological Effects of FLASH Irradiation.Antioxidants (Basel, Switzerland) · 2025Review
- FLASH radiotherapy spares lymphocytes in tumor-draining lymph nodes and increases infiltration of immune cells in tumors.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Recently, ultra-high dose rate (> 40 Gy/s, uHDR; FLASH) radiation therapy (RT) has attracted interest, because the FLASH effect that is, while a cell-killing effect on cancer cells remains, the damage to normal tissue could be spared has been reported. This study aimed to compare the immune-related protein expression on cancer cells after γ-ray, conventionally used dose rate (Conv) carbon ion (C-ion), and uHDR C-ion. B16F10 murine melanoma and Pan02 murine pancreas cancer were irradiated with γ-ray at Osaka University and with C-ion at Osaka HIMAK. The dose rates at 1.16 Gy/s for Conv and 380 Gy/s for uHDR irradiation. The expressed calreticulin (CRT), major histocompatibility complex class (MHC)-I, and programmed cell death 1 ligand (PD-L1) were evaluated by flow cytometry. Western blotting and PCR were utilized to evaluate endoplasmic reticulum (ER) stress, DNA damage, and its repair pathway. CRT, MHC-I on B16F10 was also increased by irradiation, while only C-ion increased MHC-I on Pan02. Notably, PD-L1 on B16F10 was increased after irradiation with both γ-ray and C-ion, while uHDR C-ion suppressed the expression of PD-L1 on Pan02. The present study indicated that uHDR C-ion has a different impact on the repair pathway of DNA damage and ER than the Conv C-ion. This is the first study to show the immune-related protein expressions on cancer cells after uHDR C-ion irradiation.
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