ArticlePloS one2011
Radiation-induced carcinogenesis: mechanistically based differences between gamma-rays and neutrons, and interactions with DMBA.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Quantifying the effects of neutron dose, dose protraction, age and sex on mouse survival using parametric regression and machine learning on a 21,000-mouse data set.Scientific reports · 2023Article
- Gene Signatures Induced by Ionizing Radiation as Prognostic Tools in an In Vitro Experimental Breast Cancer Model.Cancers · 2021Review
- Quantitative modeling of multigenerational effects of chronic ionizing radiation using targeted and nontargeted effects.Scientific reports · 2021Article
- REVIEW OF QUANTITATIVE MECHANISTIC MODELS OF RADIATION-INDUCED NON-TARGETED EFFECTS (NTE).Radiation protection dosimetry · 2020Review
- Mechanistic Modelling of Radiation Responses.Cancers · 2019Review
- Changes in gene expression as one of the key mechanisms involved in radiation-induced bystander effect.Biomedical reports · 2018Review
- Role of High-Linear Energy Transfer Radiobiology in Space Radiation Exposure Risks.International journal of particle therapy · 2018Review
- γH2AX, 53BP1 and Rad51 protein foci changes in mesenchymal stem cells during prolonged X-ray irradiation.Oncotarget · 2017Article
- Article
- Quantitative modeling of responses to chronic ionizing radiation exposure using targeted and non-targeted effects.PloS one · 2017Article
- Linking Gamma-H2AX Foci and Cancer in Rat Skin Exposed to Heavy Ions and Electron Radiation.Health physics · 2015Article
- Radiotherapy for benign disease; assessing the risk of radiation-induced cancer following exposure to intermediate dose radiation.The British journal of radiology · 2015Review
- Beyond two-stage models for lung carcinogenesis in the Mayak workers: implications for plutonium risk.PloS one · 2015Article
- Biological Effects of Space Radiation and Development of Effective Countermeasures.Life sciences in space research · 2014Article
- Effects of 28Si ions, 56Fe ions, and protons on the induction of murine acute myeloid leukemia and hepatocellular carcinoma.PloS one · 2014Article
- Second malignancies following conventional or combined ²⁵²Cf neutron brachytherapy with external beam radiotherapy for breast cancer.Journal of radiation research · 2013Article
- Defining molecular and cellular responses after low and high linear energy transfer radiations to develop biomarkers of carcinogenic risk or therapeutic outcome.Health physics · 2012Review
- CT scan: a benefit that may be evil.Brazilian journal of otorhinolaryngology · 2012Article
- Metachronous Presentation of BCL-2-Positive Lung Adenocarcinoma and Acute Myeloid Leukemia: A Case Presentation and Review of the Literature.Case reports in oncologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Different types of ionizing radiation produce different dependences of cancer risk on radiation dose/dose rate. Sparsely ionizing radiation (e.g. γ-rays) generally produces linear or upwardly curving dose responses at low doses, and the risk decreases when the dose rate is reduced (direct dose rate effect). Densely ionizing radiation (e.g. neutrons) often produces downwardly curving dose responses, where the risk initially grows with dose, but eventually stabilizes or decreases. When the dose rate is reduced, the risk increases (inverse dose rate effect). These qualitative differences suggest qualitative differences in carcinogenesis mechanisms. We hypothesize that the dominant mechanism for induction of many solid cancers by sparsely ionizing radiation is initiation of stem cells to a pre-malignant state, but for densely ionizing radiation the dominant mechanism is radiation-bystander-effect mediated promotion of already pre-malignant cell clone growth. Here we present a mathematical model based on these assumptions and test it using data on the incidence of dysplastic growths and tumors in the mammary glands of mice exposed to high or low dose rates of γ-rays and neutrons, either with or without pre-treatment with the chemical carcinogen 7,12-dimethylbenz-alpha-anthracene (DMBA). The model provides a mechanistic and quantitative explanation which is consistent with the data and may provide useful insight into human carcinogenesis.
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Registered trials
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.