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Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation
Epidemiological studies of atomic-bomb survivors have revealed an increased risk of lymphoid neoplasm (i.e. acute lymphoblastic leukemia) associated with radiation exposure. In particular, children are more susceptible to radiation-induced precursor lymphoid neoplasm than adults. Although ~75% of hu...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7482158/ https://www.ncbi.nlm.nih.gov/pubmed/32808021 http://dx.doi.org/10.1093/jrr/rraa055 |
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author | Tachibana, Hirotaka Morioka, Takamitsu Daino, Kazuhiro Shang, Yi Ogawa, Mari Fujita, Misuzu Matsuura, Akira Nogawa, Hiroyuki Shimada, Yoshiya Kakinuma, Shizuko |
author_facet | Tachibana, Hirotaka Morioka, Takamitsu Daino, Kazuhiro Shang, Yi Ogawa, Mari Fujita, Misuzu Matsuura, Akira Nogawa, Hiroyuki Shimada, Yoshiya Kakinuma, Shizuko |
author_sort | Tachibana, Hirotaka |
collection | PubMed |
description | Epidemiological studies of atomic-bomb survivors have revealed an increased risk of lymphoid neoplasm (i.e. acute lymphoblastic leukemia) associated with radiation exposure. In particular, children are more susceptible to radiation-induced precursor lymphoid neoplasm than adults. Although ~75% of human lymphoid tumors are B-cell neoplasms, the carcinogenic risk associated with each stage of differentiation of B-cells after radiation exposure is poorly understood. Therefore, we irradiated mice at infancy or in young adulthood to investigate the effect of age at exposure on the risk of developing B-cell neoplasms. Histopathology was used to confirm the presence of lymphoid neoplasms, and the population of B-cell neoplasms was classified into the precursor B-cell (pro-B and pre-B cell) type and mature B-cell type, according to immunophenotype. The data revealed that precursor B-cell neoplasms were induced soon after radiation exposure in infancy or young adulthood, resulting in a greater risk of developing the neoplasms. This was particularly the case for the pro-B cell type after young adult exposure. Our findings suggest that exposure to radiation at young age increases the risk of developing precursor B-cell neoplasms in humans. |
format | Online Article Text |
id | pubmed-7482158 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-74821582020-09-14 Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation Tachibana, Hirotaka Morioka, Takamitsu Daino, Kazuhiro Shang, Yi Ogawa, Mari Fujita, Misuzu Matsuura, Akira Nogawa, Hiroyuki Shimada, Yoshiya Kakinuma, Shizuko J Radiat Res Regular Paper Epidemiological studies of atomic-bomb survivors have revealed an increased risk of lymphoid neoplasm (i.e. acute lymphoblastic leukemia) associated with radiation exposure. In particular, children are more susceptible to radiation-induced precursor lymphoid neoplasm than adults. Although ~75% of human lymphoid tumors are B-cell neoplasms, the carcinogenic risk associated with each stage of differentiation of B-cells after radiation exposure is poorly understood. Therefore, we irradiated mice at infancy or in young adulthood to investigate the effect of age at exposure on the risk of developing B-cell neoplasms. Histopathology was used to confirm the presence of lymphoid neoplasms, and the population of B-cell neoplasms was classified into the precursor B-cell (pro-B and pre-B cell) type and mature B-cell type, according to immunophenotype. The data revealed that precursor B-cell neoplasms were induced soon after radiation exposure in infancy or young adulthood, resulting in a greater risk of developing the neoplasms. This was particularly the case for the pro-B cell type after young adult exposure. Our findings suggest that exposure to radiation at young age increases the risk of developing precursor B-cell neoplasms in humans. Oxford University Press 2020-08-18 /pmc/articles/PMC7482158/ /pubmed/32808021 http://dx.doi.org/10.1093/jrr/rraa055 Text en © The Author(s) 2020. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Radiation Oncology. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Regular Paper Tachibana, Hirotaka Morioka, Takamitsu Daino, Kazuhiro Shang, Yi Ogawa, Mari Fujita, Misuzu Matsuura, Akira Nogawa, Hiroyuki Shimada, Yoshiya Kakinuma, Shizuko Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation |
title | Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation |
title_full | Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation |
title_fullStr | Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation |
title_full_unstemmed | Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation |
title_short | Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation |
title_sort | early induction and increased risk of precursor b-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation |
topic | Regular Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7482158/ https://www.ncbi.nlm.nih.gov/pubmed/32808021 http://dx.doi.org/10.1093/jrr/rraa055 |
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