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Monitoring exposure to atomic bomb radiation by somatic mutation.

Atomic bomb survivors are a population suitable for studying the relationship between somatic mutation and cancer risk because their exposure doses are relatively well known and their dose responses in terms of cancer risk have also been thoroughly studied. An analysis has been made of erythrocyte g...

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Autores principales: Akiyama, M, Kyoizumi, S, Kusunoki, Y, Hirai, Y, Tanabe, K, Cologne, J B
Formato: Texto
Lenguaje:English
Publicado: 1996
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1469618/
https://www.ncbi.nlm.nih.gov/pubmed/8781371
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author Akiyama, M
Kyoizumi, S
Kusunoki, Y
Hirai, Y
Tanabe, K
Cologne, J B
author_facet Akiyama, M
Kyoizumi, S
Kusunoki, Y
Hirai, Y
Tanabe, K
Cologne, J B
author_sort Akiyama, M
collection PubMed
description Atomic bomb survivors are a population suitable for studying the relationship between somatic mutation and cancer risk because their exposure doses are relatively well known and their dose responses in terms of cancer risk have also been thoroughly studied. An analysis has been made of erythrocyte glycophorin A (GPA) gene mutations in 1,226 atomic bomb survivors in Hiroshima and Nagasaki. The GPA mutation frequency (Mf) increased slightly but significantly with age at the time of measurement and with the number of cigarettes smoked. After adjustment for the effect of smoking, the Mf was significantly higher in males than in females and higher in Hiroshima than in Nagasaki. All of these characteristics of the background GPA Mf were in accord with those of solid tumor incidence obtained from an earlier epidemiological study of A-bomb survivors. Analysis of the dose effect on Mf revealed the doubling dose to be about 1.20 Sv and the minimum dose for detection of a significant increase to be about 0.24 Sv. No significant dose effect for difference in sex, city, or age at the time of bombing was observed. Interestingly, the doubling dose for the GPA Mf approximated that for solid cancer incidence (1.59 Sv). And the minimum dose for detection was not inconsistent with the data for solid cancer incidence. The dose effect was significantly higher in those diagnosed with cancer before or after measurement than in those without a history of cancer. These findings are consistent with the hypothesis that somatic mutations are the main cause of excess cancer risk from radiation exposure.
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spelling pubmed-14696182006-06-01 Monitoring exposure to atomic bomb radiation by somatic mutation. Akiyama, M Kyoizumi, S Kusunoki, Y Hirai, Y Tanabe, K Cologne, J B Environ Health Perspect Research Article Atomic bomb survivors are a population suitable for studying the relationship between somatic mutation and cancer risk because their exposure doses are relatively well known and their dose responses in terms of cancer risk have also been thoroughly studied. An analysis has been made of erythrocyte glycophorin A (GPA) gene mutations in 1,226 atomic bomb survivors in Hiroshima and Nagasaki. The GPA mutation frequency (Mf) increased slightly but significantly with age at the time of measurement and with the number of cigarettes smoked. After adjustment for the effect of smoking, the Mf was significantly higher in males than in females and higher in Hiroshima than in Nagasaki. All of these characteristics of the background GPA Mf were in accord with those of solid tumor incidence obtained from an earlier epidemiological study of A-bomb survivors. Analysis of the dose effect on Mf revealed the doubling dose to be about 1.20 Sv and the minimum dose for detection of a significant increase to be about 0.24 Sv. No significant dose effect for difference in sex, city, or age at the time of bombing was observed. Interestingly, the doubling dose for the GPA Mf approximated that for solid cancer incidence (1.59 Sv). And the minimum dose for detection was not inconsistent with the data for solid cancer incidence. The dose effect was significantly higher in those diagnosed with cancer before or after measurement than in those without a history of cancer. These findings are consistent with the hypothesis that somatic mutations are the main cause of excess cancer risk from radiation exposure. 1996-05 /pmc/articles/PMC1469618/ /pubmed/8781371 Text en
spellingShingle Research Article
Akiyama, M
Kyoizumi, S
Kusunoki, Y
Hirai, Y
Tanabe, K
Cologne, J B
Monitoring exposure to atomic bomb radiation by somatic mutation.
title Monitoring exposure to atomic bomb radiation by somatic mutation.
title_full Monitoring exposure to atomic bomb radiation by somatic mutation.
title_fullStr Monitoring exposure to atomic bomb radiation by somatic mutation.
title_full_unstemmed Monitoring exposure to atomic bomb radiation by somatic mutation.
title_short Monitoring exposure to atomic bomb radiation by somatic mutation.
title_sort monitoring exposure to atomic bomb radiation by somatic mutation.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1469618/
https://www.ncbi.nlm.nih.gov/pubmed/8781371
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