Pathological point of view on the atomic bomb-related solid cancers.
Gespeichert in:
| Titel: | Pathological point of view on the atomic bomb-related solid cancers. |
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| Autoren: | Nakashima M; Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan.; Tissue and Histopathology Section, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan.; Thyroid Cancer Collaborative Research Center, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan., Kurohama H; Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan.; Tissue and Histopathology Section, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan.; Thyroid Cancer Collaborative Research Center, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki 852-8523, Japan., Akazawa Y; Department of Histology and Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan. |
| Quelle: | Carcinogenesis [Carcinogenesis] 2025 Sep 04; Vol. 46 (3). |
| Publikationsart: | Journal Article; Review |
| Sprache: | English |
| Info zur Zeitschrift: | Publisher: Irl Press At Oxford University Press Country of Publication: England NLM ID: 8008055 Publication Model: Print Cited Medium: Internet ISSN: 1460-2180 (Electronic) Linking ISSN: 01433334 NLM ISO Abbreviation: Carcinogenesis Subsets: MEDLINE |
| Imprint Name(s): | Publication: Oxford : Irl Press At Oxford University Press Original Publication: [New York, IRL Press] |
| MeSH-Schlagworte: | Neoplasms, Radiation-Induced*/pathology , Neoplasms, Radiation-Induced*/etiology , Neoplasms, Radiation-Induced*/epidemiology , Neoplasms, Radiation-Induced*/genetics , Nuclear Weapons*, Humans ; Animals ; Genomic Instability/radiation effects ; Atomic Bomb Survivors ; DNA Damage ; Carcinogenesis/radiation effects ; Carcinogenesis/genetics |
| Abstract: | Competing Interests: Conflict of interest: None of the authors have any potential conflicts of interest associated with this research. Eighty years have passed since the atomic bombings (A-bombing) of Hiroshima and Nagasaki in August 1945. Survivors represent an unparalleled and irreplaceable human cohort for comprehensively studying the long-term carcinogenic effects of radiation exposure. This review provides a pathological perspective on A-bomb radiation-related solid cancers. Key findings underscore the persistent nature of radiation-induced carcinogenesis: an increased risk of solid cancers has been evident for over 10 years post-bombing and continues to persist. Epidemiological data consistently demonstrate a linear dose-response relationship, with the risk of all solid cancers increasing by ∼40%-50% per Gy, notably without an apparent threshold. The phenomenon of multiple primary cancers is significantly affected by A-bomb radiation, suggesting a systemic predisposition. At a molecular level, evidence points to long-lasting genomic instability, characterized by constitutive activation of the DNA damage response in non-neoplastic epidermis of proximally exposed survivors. This persistent genomic disruption is a critical contributing factor to tumorigenesis. Furthermore, radiation-associated cancers exhibit distinct molecular features. For instance, specific gene fusions are prevalent in thyroid cancer, while HER2 and c-MYC co-amplifications are observed in breast cancer, and gene expression alterations are noted in gastric cancer, often differing from sporadic cases. Research into biomarkers, such as cdkn1a in a rat model of thyroid carcinogenesis, shows promise for identifying radiation effects from the early pre-cancerous phase. This comprehensive analysis highlights the profound and enduring impact of A-bomb radiation on human carcinogenesis. The insights derived from this unique cohort are profoundly relevant for understanding and mitigating global radiation health risks. (© The Author(s) 2025. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.) |
| Grant Information: | 23K06465 Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Science, Sports, and Culture; 20K07424 Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Science, Sports, and Culture; 16K08714 Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Science, Sports, and Culture; 19K07463 Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Science, Sports, and Culture; Atomic Bomb Disease Institute, Nagasaki University; Program of the Network-Type Joint Usage/Research Center for Radiation Disaster Medical Science |
| Contributed Indexing: | Keywords: Atomic bomb survivors; carcinogenesis; pathology; radiation; solid cancer |
| Entry Date(s): | Date Created: 20251118 Date Completed: 20251118 Latest Revision: 20251118 |
| Update Code: | 20251119 |
| DOI: | 10.1093/carcin/bgaf072 |
| PMID: | 41252537 |
| Datenbank: | MEDLINE |
Nájsť tento článok vo Web of Science | Abstract: | Competing Interests: Conflict of interest: None of the authors have any potential conflicts of interest associated with this research.<br />Eighty years have passed since the atomic bombings (A-bombing) of Hiroshima and Nagasaki in August 1945. Survivors represent an unparalleled and irreplaceable human cohort for comprehensively studying the long-term carcinogenic effects of radiation exposure. This review provides a pathological perspective on A-bomb radiation-related solid cancers. Key findings underscore the persistent nature of radiation-induced carcinogenesis: an increased risk of solid cancers has been evident for over 10 years post-bombing and continues to persist. Epidemiological data consistently demonstrate a linear dose-response relationship, with the risk of all solid cancers increasing by ∼40%-50% per Gy, notably without an apparent threshold. The phenomenon of multiple primary cancers is significantly affected by A-bomb radiation, suggesting a systemic predisposition. At a molecular level, evidence points to long-lasting genomic instability, characterized by constitutive activation of the DNA damage response in non-neoplastic epidermis of proximally exposed survivors. This persistent genomic disruption is a critical contributing factor to tumorigenesis. Furthermore, radiation-associated cancers exhibit distinct molecular features. For instance, specific gene fusions are prevalent in thyroid cancer, while HER2 and c-MYC co-amplifications are observed in breast cancer, and gene expression alterations are noted in gastric cancer, often differing from sporadic cases. Research into biomarkers, such as cdkn1a in a rat model of thyroid carcinogenesis, shows promise for identifying radiation effects from the early pre-cancerous phase. This comprehensive analysis highlights the profound and enduring impact of A-bomb radiation on human carcinogenesis. The insights derived from this unique cohort are profoundly relevant for understanding and mitigating global radiation health risks.<br /> (© The Author(s) 2025. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.) |
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| ISSN: | 1460-2180 |
| DOI: | 10.1093/carcin/bgaf072 |