Cell death pathways in directly irradiated cells and cells exposed to medium from irradiated cells

Jella, Kishore Kumar; Garcia, Amaya; McClean, Brendan; Byrne, Hugh J.; Lyng, Fiona M.

doi:10.3109/09553002.2013.734942

Cited by 21 publications

(12 citation statements)

References 43 publications

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“…Consequently, cancer cells containing unrepaired DNA enter prematurely into mitosis and undergo mitotic catastrophe (5). In addition, the irradiation of human keratinocytes with doses ranging from 0.005 to 0.5 Gy induces early apoptosis and necrosis with a substantial population of cells that undergo G2/M arrest and ultimately die through mitotic cell death (20), indicating that non-tumoral cells may also undergo a mitotic death after IR. Alternatively, mitotic catastrophe may result from the hyper-amplification of centrosomes as a result of failure to repair the DNA damages induced by IR, and lead to multipolar mitotic spindles and abnormal chromosomal segregation (21).…”

Section: Ionizing Radiation Dictates the Death And The Immunogenicitymentioning

confidence: 99%

Modulating Both Tumor Cell Death and Innate Immunity Is Essential for Improving Radiation Therapy Effectiveness

Allouch

Martins

et al. 2017

Front. Immunol.

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Radiation therapy is one of the cornerstones of cancer treatment. In tumor cells, exposure to ionizing radiation (IR) provokes DNA damages that trigger various forms of cell death such as apoptosis, necrosis, autophagic cell death, and mitotic catastrophe. IR can also induce cellular senescence that could serve as an additional antitumor barrier in a context-dependent manner. Moreover, accumulating evidence has demonstrated that IR interacts profoundly with tumor-infiltrating immune cells, which cooperatively drive treatment outcomes. Recent preclinical and clinical successes due to the combination of radiation therapy and immune checkpoint blockade have underscored the need for a better understanding of the interplay between radiation therapy and the immune system. In this review, we will present an overview of cell death modalities induced by IR, summarize the immunogenic properties of irradiated cancer cells, and discuss the biological consequences of IR on innate immune cell functions, with a particular attention on dendritic cells, macrophages, and NK cells. Finally, we will discuss their potential applications in cancer treatment.

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Section: Ionizing Radiation Dictates the Death And The Immunogenicitymentioning

confidence: 99%

Modulating Both Tumor Cell Death and Innate Immunity Is Essential for Improving Radiation Therapy Effectiveness

Allouch

Martins

et al. 2017

Front. Immunol.

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“…Apoptosis was found to be increased in the non-targeted cells [46][47][48][49], as were steps in the apoptotic pathway such as calcium flux, mitochondrial membrane depolarisation, caspase 3 release etc. [50][51][52].…”

Section: B Possible Reasons/mechanismsmentioning

confidence: 99%

Relevance of Non-Targeted Effects for Radiotherapy and Diagnostic Radiology

Mothersill¹,

Rusin²,

Seymour³

2019

Preprint

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Non-targeted effects (NTE) such as bystander effects or genomic instability have been known for many years but their significance for radiotherapy or medical diagnostic radiology are far from clear. Central to the issue are reported differences in response of normal and tumour tissues to signals from directly irradiated cells. This review will discuss possible mechanisms and implications of these different responses and will then discuss possible new therapeutic avenues suggested by the analysis. Finally, the importance of NTE for diagnostic radiology and nuclear medicine which stems from the dominance of NTE in the low dose region of the dose response curve will be presented. Areas such as second cancer induction and microenvironment plasticity will be discussed.

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“…Necrosis typically results from a higher magnitude of stress relative to either apoptosis or cellular senescence [31,131,133], and radiation-induced necrosis has been demonstrated in vitro and in vivo [134–137]. For example, high radiation exposures (≥ 32–50 Gy) were demonstrated to induce necrosis in neurons and in p53-deficient human leukemia cells in cell culture [11,138].…”

Section: Ionizing Radiation-induced Cell Toxicitiesmentioning

confidence: 99%

“…For example, high radiation exposures (≥ 32–50 Gy) were demonstrated to induce necrosis in neurons and in p53-deficient human leukemia cells in cell culture [11,138]. However, lower doses of gamma radiation (0.5 Gy) were shown to cause necrosis in the immortalized human keratinocyte cell line HaCaT [137]. In contrast to apoptosis , necrosis (including radiation-induced necrosis) is associated with increased inflammation of the surrounding normal tissue [8,139].…”

Section: Ionizing Radiation-induced Cell Toxicitiesmentioning

confidence: 99%

Mechanisms of Radiation Toxicity in Transformed and Non-Transformed Cells

Panganiban

Snow

Day

2013

IJMS

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Radiation damage to biological systems is determined by the type of radiation, the total dosage of exposure, the dose rate, and the region of the body exposed. Three modes of cell death—necrosis, apoptosis, and autophagy—as well as accelerated senescence have been demonstrated to occur in vitro and in vivo in response to radiation in cancer cells as well as in normal cells. The basis for cellular selection for each mode depends on various factors including the specific cell type involved, the dose of radiation absorbed by the cell, and whether it is proliferating and/or transformed. Here we review the signaling mechanisms activated by radiation for the induction of toxicity in transformed and normal cells. Understanding the molecular mechanisms of radiation toxicity is critical for the development of radiation countermeasures as well as for the improvement of clinical radiation in cancer treatment.

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Cell death pathways in directly irradiated cells and cells exposed to medium from irradiated cells

Abstract: CitationJella

Cited by 21 publications

References 43 publications

Modulating Both Tumor Cell Death and Innate Immunity Is Essential for Improving Radiation Therapy Effectiveness

Modulating Both Tumor Cell Death and Innate Immunity Is Essential for Improving Radiation Therapy Effectiveness

Relevance of Non-Targeted Effects for Radiotherapy and Diagnostic Radiology

Mechanisms of Radiation Toxicity in Transformed and Non-Transformed Cells

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