Non-targeted effects and radiation-induced carcinogenesis: a review

Burtt, Julie; Thompson, Patsy; Lafrenie, Robert M.

doi:10.1088/0952-4746/36/1/r23

Cited by 35 publications

(34 citation statements)

References 116 publications

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“…However, an optimal RT regimen is still not clear and under current discussion [ 54 ]. Additionally, due to discussion about a possible carcinogenic late risk, the application of LD-RT is still a subject of controversial debate and less accepted in many countries [ 55 , 56 ]. For these reasons, a reduction in radiation doses in LD-RT is an impact of many efforts both clinically and experimentally.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Inflammatory Reactions by Low-Dose Ionizing Radiation: Cytokine Release of Murine Endothelial Cells Is Dependent on Culture Conditions

Schröder

Kriesen

Paape

et al. 2018

Journal of Immunology Research

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Background In many European countries, patients with a variety of chronical inflammatory diseases are treated with low-dose radiotherapy (LD-RT). In contrast to high-dose irradiation given to tumor patients, little is known about radiobiological mechanisms underlying this clinical successful LD-RT application. The objective of this study was to gain a better insight into the modulation of inflammatory reactions after LD-RT on the basis of endothelial cells (EC) as major participants and regulators of inflammation. Methods Three murine EC lines were cultivated under 2D and 3D culture conditions and irradiated with doses from 0.01 Gy to 2 Gy. To simulate an inflammatory situation, cells were activated with TNF-α. After LD-RT, a screening of numerous inflammatory markers was determined by multiplex assay, followed by detailed analyses of four cytokines (KC, MCP-1, RANTES, and G-CSF). Additionally, the monocyte binding to EC was analyzed. Results Cytokine concentrations were dependent on culture condition, IR dose, time point after IR, and EC origin. IR caused nonlinear dose-dependent effects on secretion of the proinflammatory cytokines KC, MCP-1, and RANTES. The monocyte adhesion was significantly enhanced after IR as well as activation. Conclusions The study shows that LD-RT, also using very low radiation doses, has a clear immunomodulatory effect on EC as major participants and regulators of inflammation.

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Section: Discussionmentioning

confidence: 99%

Modulation of Inflammatory Reactions by Low-Dose Ionizing Radiation: Cytokine Release of Murine Endothelial Cells Is Dependent on Culture Conditions

Schröder

Kriesen

Paape

et al. 2018

Journal of Immunology Research

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“…This vicious relationship which is usually accompanied by GI can be considered without any doubt as the major pathway leading to carcinogenesis [ 144 , 145 ]. Chronic inflammation which is synonymous to the activation of innate immune system can lead to the downregulation of DNA repair pathways and cell cycle checkpoints due to the release of inflammatory mediators and ROS which can lead to GI [ 146 ]. Towards this direction, Colotta et al suggested a few years ago, that cancer-related inflammation can promote GI by the various inflammatory mediators, leading to accumulation of random genetic modification in cancer or healthy cells.…”

Section: Resultsmentioning

confidence: 99%

Complex DNA Damage: A Route to Radiation-Induced Genomic Instability and Carcinogenesis

Mavragani

Nikitaki

Souli

et al. 2017

Cancers

130

111

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Cellular effects of ionizing radiation (IR) are of great variety and level, but they are mainly damaging since radiation can perturb all important components of the cell, from the membrane to the nucleus, due to alteration of different biological molecules ranging from lipids to proteins or DNA. Regarding DNA damage, which is the main focus of this review, as well as its repair, all current knowledge indicates that IR-induced DNA damage is always more complex than the corresponding endogenous damage resulting from endogenous oxidative stress. Specifically, it is expected that IR will create clusters of damage comprised of a diversity of DNA lesions like double strand breaks (DSBs), single strand breaks (SSBs) and base lesions within a short DNA region of up to 15–20 bp. Recent data from our groups and others support two main notions, that these damaged clusters are: (1) repair resistant, increasing genomic instability (GI) and malignant transformation and (2) can be considered as persistent “danger” signals promoting chronic inflammation and immune response, causing detrimental effects to the organism (like radiation toxicity). Last but not least, the paradigm shift for the role of radiation-induced systemic effects is also incorporated in this picture of IR-effects and consequences of complex DNA damage induction and its erroneous repair.

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“…Together, the authors estimate this would result in up to 4000 excess fatal malignancies all together [ 13 ]. Radiation has a stochastic effect meaning that any dose of radiation may lead to the development of malignancy, though higher doses having an increasingly linear dose-effect relationship [ 14 ]. Despite these findings, statistical models do not show evidence that cardiac catheterization leads to the development of malignancy.…”

Section: Discussionmentioning

confidence: 99%

Radiation-Induced Sarcoma following Prolonged Coronary Stent Placement

Vick

Clark

Lewis

2018

Case Reports in Surgery

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Radiation exposure for the average coronary stent placement varies based on a number of factors but typically amounts to 6–11 mSv per patient (compared to 3 mSv background). As with all procedures which utilize radiation, there is an inherent risk of genetic mutation and the possible development of malignancy. Here, we present the case of a 75-year-old male who presented with an exophytic mass on his back following prolonged coronary catheterization with a radiation burn seven years prior. Biopsy of the lesion revealed the mass was consistent with an undifferentiated pleomorphic sarcoma emanating from the site of the radiation burn. After staging studies demonstrated no evidence of metastatic disease, radical excision with negative margins was performed. This case demonstrates that despite the rarity of radiation injury, each incidence necessitates strict monitoring of radiation exposure and continual follow-up due to the risk of malignancy.

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Non-targeted effects and radiation-induced carcinogenesis: a review

Cited by 35 publications

References 116 publications

Modulation of Inflammatory Reactions by Low-Dose Ionizing Radiation: Cytokine Release of Murine Endothelial Cells Is Dependent on Culture Conditions

Modulation of Inflammatory Reactions by Low-Dose Ionizing Radiation: Cytokine Release of Murine Endothelial Cells Is Dependent on Culture Conditions

Complex DNA Damage: A Route to Radiation-Induced Genomic Instability and Carcinogenesis

Radiation-Induced Sarcoma following Prolonged Coronary Stent Placement

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