
Early induction and increased risk of precursor B-cell neoplasms after exposure of infant or young-adult mice to ionizing radiation
Author(s) -
Hirotaka Tachibana,
Takamitsu Morioka,
Kazuhiro Daino,
Yi Shang,
Mari Ogawa,
Misuzu Fujita,
Akira Matsuura,
Hiroyuki Nogawa,
Yoshiya Shimada,
Shizuko Kakinuma
Publication year - 2020
Publication title -
journal of radiation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.643
H-Index - 60
eISSN - 1349-9157
pISSN - 0449-3060
DOI - 10.1093/jrr/rraa055
Subject(s) - immunophenotyping , neoplasm , carcinogen , ionizing radiation , pathology , b cell , cell , radiation exposure , population , medicine , leukemia , biology , immunology , physiology , antibody , genetics , antigen , irradiation , environmental health , nuclear medicine , physics , nuclear physics
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.