Repair of DNA damage induced by ionizing radiation and benzo[α]pyrene in mammalian cells

1977 ◽  
Vol 2 (6) ◽  
pp. 1375-1386 ◽  
Author(s):  
Peter Cerutti ◽  
Kunio Shinohara ◽  
Joyce Remsen
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Mammalian Cells

scholarly journals Interaction between Fibroblasts and Immune Cells Following DNA Damage Induced by Ionizing Radiation

2020 ◽  
Author(s):  
Kalaiyarasi Ragunathan ◽  
Nikki Lyn Esnardo Upfold ◽  
Valentyn Oksenych
Keyword(s):  
Dna Damage ◽  
Tumor Microenvironment ◽  
Ionizing Radiation ◽  
Immune Cells ◽  
Mammalian Cells ◽  
Cancer Associated Fibroblasts ◽  
Cell Type ◽  
Dna Damages ◽  
Damage Response ◽  
High Doses

Cancer-associated fibroblasts (CAF) form the basis of tumor microenvironment and possess immunomodulatory functions by interacting with other cells surrounding tumor, including T lymphocytes, macrophages, dendritic cells and natural killer cells. Ionizing radiation is a broadly-used method in radiotherapy to target tumors. In mammalian cells, ionizing radiation induces various types of DNA damages and DNA damage response. Being unspecific, radiotherapy affects all the cells in tumor microenvironment, including the tumor itself, CAFs and immune cells. CAFs are extremely radio-resistant and do not initiate apoptosis even at high doses of radiation. However, following radiation, CAFs become senescent and produce a distinct combination of immunoregulatory molecules. Radiosensitivity of immune cells varies depending on the cell type due to inefficient DNA repair in, for example, monocytes and granulocytes. In this minireview, we are summarizing recent findings on the interaction between CAF, ionizing radiation and immune cells in the tumor microenvironment.

On the regulation of the p53 tumour suppressor, and its role in the cellular response to DNA damage

1995 ◽  
Vol 347 (1319) ◽  
pp. 83-87 ◽  
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Mammalian Cells ◽  
Cellular Response ◽  
P53 Gene ◽  
Viral Proteins ◽  
Biologically Active ◽  
Discrete Control ◽  
Apoptotic Response ◽  
P53 Activation

The p53 gene is required for the normal apoptotic response of mammalian cells to DNA damage caused by ionizing radiation and DNA damaging drugs. DNA damage results in the accumulation of biologically active p53. This response is potentially lethal and is therefore highly regulated. By using both biochemical and cell biological approaches a number of discrete control pathways have been identified. These include analysis of cellular and viral proteins that bind to p53 to inactivate its function, the discovery of cells with defects in the p53 activation pathway and the analysis of an allosteric regulation of p53 function controlled by phosphorylation.

scholarly journals Interaction between Fibroblasts and Immune Cells Following DNA Damage Induced by Ionizing Radiation

2020 ◽  
Author(s):  
Valentyn Oksenych
Keyword(s):  
Dna Damage ◽  
Tumor Microenvironment ◽  
Ionizing Radiation ◽  
Immune Cells ◽  
Mammalian Cells ◽  
Cancer Associated Fibroblasts ◽  
Cell Type ◽  
Dna Damages ◽  
Damage Response ◽  
High Doses

Cancer-associated fibroblasts (CAF) form the basis of tumor microenvironment and possess immunomodulatory functions by interacting with other cells surrounding tumor, including T lymphocytes, macrophages, dendritic cells and natural killer cells. Ionizing radiation is a broadly-used method in radiotherapy to target tumors. In mammalian cells, ionizing radiation induces various types of DNA damages and DNA damage response. Being unspecific, radiotherapy affects all the cells in tumor microenvironment, including the tumor itself, CAFs and immune cells. CAFs are extremely radio-resistant and do not initiate apoptosis even at high doses of radiation. However, following radiation, CAFs become senescent and produce a distinct combination of immunoregulatory molecules. Radiosensitivity of immune cells varies depending on the cell type due to inefficient DNA repair in, for example, monocytes and granulocytes. In this minireview, we are summarizing recent findings on the interaction between CAF, ionizing radiation and immune cells in the tumor microenvironment.

scholarly journals Interaction between Fibroblasts and Immune Cells Following DNA Damage Induced by Ionizing Radiation

2020 ◽  
Vol 21 (22) ◽  
pp. 8635 ◽  
Author(s):  
Kalaiyarasi Ragunathan ◽  
Nikki Lyn Esnardo Upfold ◽  
Valentyn Oksenych
Keyword(s):  
Dna Damage ◽  
Tumor Microenvironment ◽  
Ionizing Radiation ◽  
Immune Cells ◽  
Mammalian Cells ◽  
Cancer Associated Fibroblasts ◽  
Cell Type ◽  
Dna Damages ◽  
Damage Response ◽  
High Doses

Cancer-associated fibroblasts (CAF) form the basis of tumor microenvironment and possess immunomodulatory functions by interacting with other cells surrounding tumor, including T lymphocytes, macrophages, dendritic cells and natural killer cells. Ionizing radiation is a broadly-used method in radiotherapy to target tumors. In mammalian cells, ionizing radiation induces various types of DNA damages and DNA damage response. Being unspecific, radiotherapy affects all the cells in tumor microenvironment, including the tumor itself, CAFs and immune cells. CAFs are extremely radio-resistant and do not initiate apoptosis even at high doses of radiation. However, following radiation, CAFs become senescent and produce a distinct combination of immunoregulatory molecules. Radiosensitivity of immune cells varies depending on the cell type due to inefficient DNA repair in, for example, monocytes and granulocytes. In this minireview, we are summarizing recent findings on the interaction between CAF, ionizing radiation and immune cells in the tumor microenvironment.

scholarly journals Mutational impact and signature of ionizing radiation

2021 ◽  
Author(s):  
Jeonghwan Youk ◽  
Hyun Woo Kwon ◽  
Joonoh Lim ◽  
Eunji Kim ◽  
Ryul Kim ◽  
...  
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Mammalian Cells ◽  
Single Cells ◽  
Dna Double Strand Breaks ◽  
Structural Variations ◽  
Dna Damage And Repair ◽  
Repair Processes ◽  
Massive Number ◽  
Chaotic Nature

AbstractWhole-genome sequencing (WGS) of human tumors and normal cells exposed to various carcinogens has revealed distinct mutational patterns that provide deep insights into the DNA damage and repair processes. Although ionizing radiation (IR) is conventionally known as a strong carcinogen, its genome-wide mutational impacts have not been comprehensively investigated at the single-nucleotide level. Here, we explored the mutational landscape of normal single-cells after exposure to the various levels of IR. On average, 1 Gy of IR exposure generated ∼16 mutational events with a spectrum consisting of predominantly small nucleotide deletions and a few characteristic structural variations. In ∼30% of the post-irradiated cells, complex genomic rearrangements, such as chromoplexy, chromothripsis, and breakage-fusion-bridge cycles, were resulted, indicating the stochastic and chaotic nature of DNA repair in the presence of the massive number of concurrent DNA double-strand breaks. These mutational signatures were confirmed in the genomes of 22 IR-induced secondary malignancies. With high-resolution genomic snapshots of irradiated cells, our findings provide deep insights into how IR-induced DNA damage and subsequent repair processes operate in mammalian cells.

scholarly journals Monte Carlo Simulation-Based Calculations of Complex DNA Damage for Incidents of Environmental Ionizing Radiation Exposure

2021 ◽  
Vol 11 (19) ◽  
pp. 8985
Author(s):  
Spyridon A. Kalospyros ◽  
Violeta Gika ◽  
Zacharenia Nikitaki ◽  
Antigoni Kalamara ◽  
Ioanna Kyriakou ◽  
...  
Keyword(s):  
Dna Damage ◽  
Monte Carlo ◽  
Ionizing Radiation ◽  
Mammalian Cells ◽  
Absorbed Dose ◽  
Dna Lesions ◽  
Lifetime Cancer Risk ◽  
Exposed Population ◽  
Exposed Individual ◽  
Risk Of Cancer

In this paper, we present a useful Monte Carlo (MC)-based methodology that can be utilized to calculate the absorbed dose and the initial levels of complex DNA damage (such as double strand breaks-DSBs) in the case of an environmental ionizing radiation (IR) exposure incident (REI) i.e., a nuclear accident. Our objective is to assess the doses and complex DNA damage by isolating only one component of the total radiation released in the environment after a REI that will affect the health of the exposed individual. More specifically, the radiation emitted by radionuclide 137Cs in the ground (under the individual’s feet). We use a merging of the Monte Carlo N-Particle Transport code (MCNP) with the Monte Carlo Damage Simulation (MCDS) code. The DNA lesions have been estimated through simulations for different surface activities of a 137Cs ground-based γ radiation source. The energy spectrum of the emitted secondary electrons and the absorbed dose in typical mammalian cells have been calculated using the MCNP code, and then these data are used as an input in the MCDS code for the estimation of critical DNA damage levels and types. As a realistic application, the calculated dose is also used to assess the Excess Lifetime Cancer Risk (ELCR) for eight hypothetical individuals, living in different zones around the Chernobyl Nuclear Power Plant, exposed to different time periods at the days of the accident in 1986. We conclude that any exposition of an individual in the near zone of Chernobyl increases the risk of cancer at a moderate to high grade, connected also with the induction of complex DNA damage by radiation. Generally, our methodology has proven to be useful for assessing γ rays-induced complex DNA damage levels of the exposed population, in the case of a REI and for better understanding the long-term health effects of exposure of the population to IR.

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