Clustered DNA double-strand break formation and the repair pathway following heavy-ion irradiation
Abstract Photons, such as X- or γ-rays, induce DNA damage (distributed throughout the nucleus) as a result of low-density energy deposition. In contrast, particle irradiation with high linear energy transfer (LET) deposits high-density energy along the particle track. High-LET heavy-ion irradiation...
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| Published in | Journal of radiation research Vol. 60; no. 1; pp. 69 - 79 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Oxford University Press
01.01.2019
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Abstract
Photons, such as X- or γ-rays, induce DNA damage (distributed throughout the nucleus) as a result of low-density energy deposition. In contrast, particle irradiation with high linear energy transfer (LET) deposits high-density energy along the particle track. High-LET heavy-ion irradiation generates a greater number and more complex critical chromosomal aberrations, such as dicentrics and translocations, compared with X-ray or γ irradiation. In addition, the formation of >1000 bp deletions, which is rarely observed after X-ray irradiation, has been identified following high-LET heavy-ion irradiation. Previously, these chromosomal aberrations have been thought to be the result of misrepair of complex DNA lesions, defined as DNA damage through DNA double-strand breaks (DSBs) and single-strand breaks as well as base damage within 1–2 helical turns (<3–4 nm). However, because the scale of complex DNA lesions is less than a few nanometers, the large-scale chromosomal aberrations at a micrometer level cannot be simply explained by complex DNA lesions. Recently, we have demonstrated the existence of clustered DSBs along the particle track through the use of super-resolution microscopy. Furthermore, we have visualized high-level and frequent formation of DSBs at the chromosomal boundary following high-LET heavy-ion irradiation. In this review, we summarize the latest findings regarding the hallmarks of DNA damage structure and the repair pathway following heavy-ion irradiation. Furthermore, we discuss the mechanism through which high-LET heavy-ion irradiation may induce dicentrics, translocations and large deletions. |
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| AbstractList | Photons, such as X- or γ-rays, induce DNA damage (distributed throughout the nucleus) as a result of low-density energy deposition. In contrast, particle irradiation with high linear energy transfer (LET) deposits high-density energy along the particle track. High-LET heavy-ion irradiation generates a greater number and more complex critical chromosomal aberrations, such as dicentrics and translocations, compared with X-ray or γ irradiation. In addition, the formation of >1000 bp deletions, which is rarely observed after X-ray irradiation, has been identified following high-LET heavy-ion irradiation. Previously, these chromosomal aberrations have been thought to be the result of misrepair of complex DNA lesions, defined as DNA damage through DNA double-strand breaks (DSBs) and single-strand breaks as well as base damage within 1–2 helical turns (<3–4 nm). However, because the scale of complex DNA lesions is less than a few nanometers, the large-scale chromosomal aberrations at a micrometer level cannot be simply explained by complex DNA lesions. Recently, we have demonstrated the existence of clustered DSBs along the particle track through the use of super-resolution microscopy. Furthermore, we have visualized high-level and frequent formation of DSBs at the chromosomal boundary following high-LET heavy-ion irradiation. In this review, we summarize the latest findings regarding the hallmarks of DNA damage structure and the repair pathway following heavy-ion irradiation. Furthermore, we discuss the mechanism through which high-LET heavy-ion irradiation may induce dicentrics, translocations and large deletions. Photons, such as X- or [gamma]-rays, induce DNA damage (distributed throughout the nucleus) as a result of lowdensity energy deposition. In contrast, particle irradiation with high linear energy transfer (LET) deposits high-density energy along the particle track. High-LET heavy-ion irradiation generates a greater number and more complex critical chromosomal aberrations, such as dicentrics and translocations, compared with X-ray or [gamma] irradiation. In addition, the formation of >1000 bp deletions, which is rarely observed after X-ray irradiation, has been identified following high-LET heavy-ion irradiation. Previously, these chromosomal aberrations have been thought to be the result of misrepair of complex DNA lesions, defined as DNA damage through DNA double-strand breaks (DSBs) and single-strand breaks as well as base damage within 1-2 helical turns (<3-4 nm). However, because the scale of complex DNA lesions is less than a few nanometers, the large-scale chromosomal aberrations at a micrometer level cannot be simply explained by complex DNA lesions. Recently, we have demonstrated the existence of clustered DSBs along the particle track through the use of super-resolution microscopy. Furthermore, we have visualized high-level and frequent formation of DSBs at the chromosomal boundary following high-LET heavy-ion irradiation. In this review, we summarize the latest findings regarding the hallmarks of DNA damage structure and the repair pathway following heavy-ion irradiation. Furthermore, we discuss the mechanism through which high-LET heavy-ion irradiation may induce dicentrics, translocations and large deletions. Keywords: heavy-ion irradiation; DNA double-strand breaks; super-resolution microscopy; DSB repair pathway; cancer treatment; radiotherapy Photons, such as X- or [gamma]-rays, induce DNA damage (distributed throughout the nucleus) as a result of lowdensity energy deposition. In contrast, particle irradiation with high linear energy transfer (LET) deposits high-density energy along the particle track. High-LET heavy-ion irradiation generates a greater number and more complex critical chromosomal aberrations, such as dicentrics and translocations, compared with X-ray or [gamma] irradiation. In addition, the formation of >1000 bp deletions, which is rarely observed after X-ray irradiation, has been identified following high-LET heavy-ion irradiation. Previously, these chromosomal aberrations have been thought to be the result of misrepair of complex DNA lesions, defined as DNA damage through DNA double-strand breaks (DSBs) and single-strand breaks as well as base damage within 1-2 helical turns (<3-4 nm). However, because the scale of complex DNA lesions is less than a few nanometers, the large-scale chromosomal aberrations at a micrometer level cannot be simply explained by complex DNA lesions. Recently, we have demonstrated the existence of clustered DSBs along the particle track through the use of super-resolution microscopy. Furthermore, we have visualized high-level and frequent formation of DSBs at the chromosomal boundary following high-LET heavy-ion irradiation. In this review, we summarize the latest findings regarding the hallmarks of DNA damage structure and the repair pathway following heavy-ion irradiation. Furthermore, we discuss the mechanism through which high-LET heavy-ion irradiation may induce dicentrics, translocations and large deletions. Photons, such as X- or γ-rays, induce DNA damage (distributed throughout the nucleus) as a result of low-density energy deposition. In contrast, particle irradiation with high linear energy transfer (LET) deposits high-density energy along the particle track. High-LET heavy-ion irradiation generates a greater number and more complex critical chromosomal aberrations, such as dicentrics and translocations, compared with X-ray or γ irradiation. In addition, the formation of >1000 bp deletions, which is rarely observed after X-ray irradiation, has been identified following high-LET heavy-ion irradiation. Previously, these chromosomal aberrations have been thought to be the result of misrepair of complex DNA lesions, defined as DNA damage through DNA double-strand breaks (DSBs) and single-strand breaks as well as base damage within 1-2 helical turns (<3-4 nm). However, because the scale of complex DNA lesions is less than a few nanometers, the large-scale chromosomal aberrations at a micrometer level cannot be simply explained by complex DNA lesions. Recently, we have demonstrated the existence of clustered DSBs along the particle track through the use of super-resolution microscopy. Furthermore, we have visualized high-level and frequent formation of DSBs at the chromosomal boundary following high-LET heavy-ion irradiation. In this review, we summarize the latest findings regarding the hallmarks of DNA damage structure and the repair pathway following heavy-ion irradiation. Furthermore, we discuss the mechanism through which high-LET heavy-ion irradiation may induce dicentrics, translocations and large deletions.Photons, such as X- or γ-rays, induce DNA damage (distributed throughout the nucleus) as a result of low-density energy deposition. In contrast, particle irradiation with high linear energy transfer (LET) deposits high-density energy along the particle track. High-LET heavy-ion irradiation generates a greater number and more complex critical chromosomal aberrations, such as dicentrics and translocations, compared with X-ray or γ irradiation. In addition, the formation of >1000 bp deletions, which is rarely observed after X-ray irradiation, has been identified following high-LET heavy-ion irradiation. Previously, these chromosomal aberrations have been thought to be the result of misrepair of complex DNA lesions, defined as DNA damage through DNA double-strand breaks (DSBs) and single-strand breaks as well as base damage within 1-2 helical turns (<3-4 nm). However, because the scale of complex DNA lesions is less than a few nanometers, the large-scale chromosomal aberrations at a micrometer level cannot be simply explained by complex DNA lesions. Recently, we have demonstrated the existence of clustered DSBs along the particle track through the use of super-resolution microscopy. Furthermore, we have visualized high-level and frequent formation of DSBs at the chromosomal boundary following high-LET heavy-ion irradiation. In this review, we summarize the latest findings regarding the hallmarks of DNA damage structure and the repair pathway following heavy-ion irradiation. Furthermore, we discuss the mechanism through which high-LET heavy-ion irradiation may induce dicentrics, translocations and large deletions. Abstract Photons, such as X- or γ-rays, induce DNA damage (distributed throughout the nucleus) as a result of low-density energy deposition. In contrast, particle irradiation with high linear energy transfer (LET) deposits high-density energy along the particle track. High-LET heavy-ion irradiation generates a greater number and more complex critical chromosomal aberrations, such as dicentrics and translocations, compared with X-ray or γ irradiation. In addition, the formation of >1000 bp deletions, which is rarely observed after X-ray irradiation, has been identified following high-LET heavy-ion irradiation. Previously, these chromosomal aberrations have been thought to be the result of misrepair of complex DNA lesions, defined as DNA damage through DNA double-strand breaks (DSBs) and single-strand breaks as well as base damage within 1–2 helical turns (<3–4 nm). However, because the scale of complex DNA lesions is less than a few nanometers, the large-scale chromosomal aberrations at a micrometer level cannot be simply explained by complex DNA lesions. Recently, we have demonstrated the existence of clustered DSBs along the particle track through the use of super-resolution microscopy. Furthermore, we have visualized high-level and frequent formation of DSBs at the chromosomal boundary following high-LET heavy-ion irradiation. In this review, we summarize the latest findings regarding the hallmarks of DNA damage structure and the repair pathway following heavy-ion irradiation. Furthermore, we discuss the mechanism through which high-LET heavy-ion irradiation may induce dicentrics, translocations and large deletions. |
| Audience | Academic |
| Author | Yamauchi, Motohiro Shibata, Atsushi Limsirichaikul, Siripan Niimi, Atsuko Nakano, Takashi Oike, Takahiro Hagiwara, Yoshihiko Sato, Hiro Held, Kathryn D |
| AuthorAffiliation | 5 Department of Radiation Oncology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA 3 Department of Radiation Biology and Protection, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan 7 Education and Research Support Center (ERSC), Graduate School of Medicine, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan 2 Research Program for Heavy Ion Therapy, Division of Integrated Oncology Research, Gunma University Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan 4 Faculty of Pharmacy, Silpakorn University, Nakhon Pathom, Thailand 1 Department of Radiation Oncology, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan 6 International Open Laboratory, Gunma University Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan |
| AuthorAffiliation_xml | – name: 3 Department of Radiation Biology and Protection, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan – name: 6 International Open Laboratory, Gunma University Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan – name: 7 Education and Research Support Center (ERSC), Graduate School of Medicine, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan – name: 4 Faculty of Pharmacy, Silpakorn University, Nakhon Pathom, Thailand – name: 1 Department of Radiation Oncology, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan – name: 2 Research Program for Heavy Ion Therapy, Division of Integrated Oncology Research, Gunma University Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan – name: 5 Department of Radiation Oncology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA |
| Author_xml | – sequence: 1 givenname: Yoshihiko surname: Hagiwara fullname: Hagiwara, Yoshihiko organization: Department of Radiation Oncology, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan – sequence: 2 givenname: Takahiro surname: Oike fullname: Oike, Takahiro organization: Department of Radiation Oncology, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan – sequence: 3 givenname: Atsuko surname: Niimi fullname: Niimi, Atsuko organization: Research Program for Heavy Ion Therapy, Division of Integrated Oncology Research, Gunma University Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan – sequence: 4 givenname: Motohiro orcidid: 0000-0001-5423-5284 surname: Yamauchi fullname: Yamauchi, Motohiro organization: Department of Radiation Biology and Protection, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan – sequence: 5 givenname: Hiro surname: Sato fullname: Sato, Hiro organization: Department of Radiation Oncology, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan – sequence: 6 givenname: Siripan surname: Limsirichaikul fullname: Limsirichaikul, Siripan organization: Faculty of Pharmacy, Silpakorn University, Nakhon Pathom, Thailand – sequence: 7 givenname: Kathryn D surname: Held fullname: Held, Kathryn D organization: Department of Radiation Oncology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA – sequence: 8 givenname: Takashi surname: Nakano fullname: Nakano, Takashi organization: Department of Radiation Oncology, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan – sequence: 9 givenname: Atsushi orcidid: 0000-0001-8912-6977 surname: Shibata fullname: Shibata, Atsushi email: shibata.at@gunma-u.ac.jp organization: Education and Research Support Center (ERSC), Graduate School of Medicine, Gunma University, 3-39-22, Showa-machi, Maebashi, Gunma, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30476166$$D View this record in MEDLINE/PubMed |
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| Copyright | The Author(s) 2018. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Radiation Oncology. 2018 COPYRIGHT 2019 Oxford University Press The Author(s) 2018. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Radiation Oncology. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | radiotherapy cancer treatment heavy-ion irradiation DNA double-strand breaks super-resolution microscopy DSB repair pathway |
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| Snippet | Abstract
Photons, such as X- or γ-rays, induce DNA damage (distributed throughout the nucleus) as a result of low-density energy deposition. In contrast,... Photons, such as X- or γ-rays, induce DNA damage (distributed throughout the nucleus) as a result of low-density energy deposition. In contrast, particle... Photons, such as X- or [gamma]-rays, induce DNA damage (distributed throughout the nucleus) as a result of lowdensity energy deposition. In contrast, particle... |
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| SubjectTerms | Aberration Cancer Chromosome abnormalities Density DNA DNA damage Energy transfer Energy transformation Gamma irradiation Gamma rays Genetic aspects Heavy ions Ion irradiation Ionizing radiation Lesions Linear energy transfer (LET) Microscopy Observations Particle tracking Radiation damage Radiation exposure Radiotherapy Review X ray irradiation |
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| Title | Clustered DNA double-strand break formation and the repair pathway following heavy-ion irradiation |
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