Radiotherapy, inflammation, and the myeloid perspective.
7 affiliations
- 1School of Biomedical Sciences and Engineering, South China University of Technology, Guangzhou International Campus, Guangzhou, China.
- 2National Engineering Research Center for Tissue Restoration and Reconstruction, Guangdong Province Key Laboratory of Biomedical Engineering, Key Laboratory of Biomedical Materials of the Ministry of Education, South China University of Technology, Guangzhou, China.
- 3Department of Neurosurgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
- 4State Key Laboratory of Molecular Oncology, Frontiers Science Center for Cancer Integrative Omics, Peking University Cancer Hospital and Institute, Peking University International Cancer Institute, Peking University Health Science Center, Beijing, China.
- 5School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China.
- 6Department of Radiation and Cellular Oncology, University of Chicago, Chicago, IL, USA.
- 7The Ludwig Center for Metastasis Research, University of Chicago, Chicago, IL, USA.
Abstract
Radiotherapy (RT) has long been regarded as a local treatment modality designed to eradicate tumor cells through targeted deoxyribonucleic acid (DNA) damage and, more recently, as an in situ vaccine capable of triggering the abscopal effect. However, increasing evidence now defines RT as a systemic immune modulatory intervention that elicits both antitumor and tumor growth-promoting effects. The recently described "badscopal effect", the paradoxical progression or growth acceleration of non-irradiated disease associated with systemic immunosuppressive and growth-factor programs initiated by the irradiated lesion, highlights that RT may, under certain inflammatory and cellular contexts, foster immune tolerance or accelerate distant disease progression. Central to this duality is the host's capacity to integrate and balance antitumor and pro-tumor responses following RT. Unlike the relatively binary activation states often attributed to T cells, myeloid cells exhibit high plasticity, integrating signals of DNA damage, hypoxia, and tissue repair to direct the inflammatory responses that inhibit or promote tumor growth. In this review, we examine how RT induces dual inflammatory programs, as a partial explanation as to why classical abscopal models incompletely capture clinical practice and how myeloid plasticity emerges as a central determinant of systemic responses to RT, with important implications for the rational design of combination therapies.
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BibTeX
@article{yang2026radiotherapy,
title = {{Radiotherapy, inflammation, and the myeloid perspective.}},
author = {Kaiting Yang and András Piffkó and Chuanhui Han and Liufu Deng and Ralph R Weichselbaum},
journal = {Medical review (2021)},
year = {2026},
month = jul,
doi = {10.1515/mr-2026-0032},
url = {https://europepmc.org/article/MED/42924312},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Radiotherapy, inflammation, and the myeloid perspective.
AU - Kaiting Yang
AU - András Piffkó
AU - Chuanhui Han
AU - Liufu Deng
AU - Ralph R Weichselbaum
PY - 2026
DA - 2026/07/01
JO - Medical review (2021)
DO - 10.1515/mr-2026-0032
UR - https://europepmc.org/article/MED/42924312
AB - Radiotherapy (RT) has long been regarded as a local treatment modality designed to eradicate tumor cells through targeted deoxyribonucleic acid (DNA) damage and, more recently, as an in situ vaccine capable of triggering the abscopal effect. However, increasing evidence now defines RT as a systemic immune modulatory intervention that elicits both antitumor and tumor growth-promoting effects. The recently described "badscopal effect", the paradoxical progression or growth acceleration of non-irradiated disease associated with systemic immunosuppressive and growth-factor programs initiated by the irradiated lesion, highlights that RT may, under certain inflammatory and cellular contexts, foster immune tolerance or accelerate distant disease progression. Central to this duality is the host's capacity to integrate and balance antitumor and pro-tumor responses following RT. Unlike the relatively binary activation states often attributed to T cells, myeloid cells exhibit high plasticity, integrating signals of DNA damage, hypoxia, and tissue repair to direct the inflammatory responses that inhibit or promote tumor growth. In this review, we examine how RT induces dual inflammatory programs, as a partial explanation as to why classical abscopal models incompletely capture clinical practice and how myeloid plasticity emerges as a central determinant of systemic responses to RT, with important implications for the rational design of combination therapies.
SN - 2097-0773
SN - 2749-9642
ER -