ArticleJournal of mathematical biology2017
A reaction-diffusion model for radiation-induced bystander effects.
Article in Journal of mathematical biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Minimising mutation load as a mechanism for low-dose hyper-radiosensitivity and induced radioresistance.Scientific reports · 2026Article
- Radiation-induced bystander effect and its clinical implications.Frontiers in oncology · 2023Review
- Datasets of in vitro clonogenic assays showing low dose hyper-radiosensitivity and induced radioresistance.Scientific data · 2022Article
- Article
- Modeling space radiation induced cognitive dysfunction using targeted and non-targeted effects.Scientific reports · 2021Article
- The Role and Mechanism of ATM-Mediated Autophagy in the Transition From Hyper-Radiosensitivity to Induced Radioresistance in Lung Cancer Under Low-Dose Radiation.Frontiers in cell and developmental biology · 2021Article
- REVIEW OF QUANTITATIVE MECHANISTIC MODELS OF RADIATION-INDUCED NON-TARGETED EFFECTS (NTE).Radiation protection dosimetry · 2020Review
- Implications of immune-mediated metastatic growth on metastatic dormancy, blow-up, early detection, and treatment.Journal of mathematical biology · 2020Article
- Hadrontherapy Interactions in Molecular and Cellular Biology.International journal of molecular sciences · 2019Review
- Effects of G2-checkpoint dynamics on low-dose hyper-radiosensitivity.Journal of mathematical biology · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We develop and analyze a reaction-diffusion model to investigate the dynamics of the lifespan of a bystander signal emitted when cells are exposed to radiation. Experimental studies by Mothersill and Seymour 1997, using malignant epithelial cell lines, found that an emitted bystander signal can still cause bystander effects in cells even 60 h after its emission. Several other experiments have also shown that the signal can persist for months and even years. Also, bystander effects have been hypothesized as one of the factors responsible for the phenomenon of low-dose hyper-radiosensitivity and increased radioresistance (HRS/IRR). Here, we confirm this hypothesis with a mathematical model, which we fit to Joiner's data on HRS/IRR in a T98G glioma cell line. Furthermore, we use phase plane analysis to understand the full dynamics of the signal's lifespan. We find that both single and multiple radiation exposure can lead to bystander signals that either persist temporarily or permanently. We also found that, in an heterogeneous environment, the size of the domain exposed to radiation and the number of radiation exposures can determine whether a signal will persist temporarily or permanently. Finally, we use sensitivity analysis to identify those cell parameters that affect the signal's lifespan and the signal-induced cell death the most.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.