2007
DOI: 10.1667/rr0763.1
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Solid Cancer Incidence in Atomic Bomb Survivors: 1958–1998

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Cited by 1,525 publications
(1,470 citation statements)
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References 99 publications
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“…In the low‐dose region, the EAR presents a linear dose–response 19, 20. Since planning CT data do not include images at larger distances for reasons of radiation protection, no calculations of the EAR based on DVH are possible, for example, bladder, bowel, and gonads.…”
Section: Methodsmentioning
confidence: 99%
See 1 more Smart Citation
“…In the low‐dose region, the EAR presents a linear dose–response 19, 20. Since planning CT data do not include images at larger distances for reasons of radiation protection, no calculations of the EAR based on DVH are possible, for example, bladder, bowel, and gonads.…”
Section: Methodsmentioning
confidence: 99%
“…EAR 0 , γ e , and γ a values have been derived by Preston et al 20. from the data of the Japanese atomic bomb survivors (EAR 0  = 0.7 per 10,000 person‐years per Gy for the brain, γ e   = −0.024, and γ a   = 2.38).…”
Section: Methodsmentioning
confidence: 99%
“…Thyroid cancer rates were observed to increase in children exposed to the atomic blasts in Japan [15].The latency period between the time of radiation exposure and cancer onset in children is typically 10-20 years [14]. More than 5,000 children developed DTC after radiation exposure after the nuclear reactor explosion tragedy at Chernobyl in 1986 [16].…”
Section: Risk Factors For Thyroid Cancer In Childrenmentioning
confidence: 99%
“…Congruent with our nonlinear findings, Preston et al, in an analysis of 42,902 men who were atomic bomb survivors, discovered that exposure to 0.5 to 1.0 grays had a parabolic-shaped relative risk curve (an inverted ''U'') with the peak incidence rate observed among men who were exposed at ages 20 to 29 years. 20 In fact, in a recent analysis of observed cancer risk patterns as a function of age at exposure in Japanese atomic bomb survivors, Brenner and colleagues described 2 separate processes that contribute to radiation-induced carcinogenesis 21 : the first is initiation, ie, the induction of irreversibly altered premalignant cells, such as mutation to an oncogene, and the second is radiation-induced promotion, ie, the process by which an initiated cell expands with a pursuant increase in the average number of premalignant stem cells per clone. Hence, whereas initiation effects are expected to be the primary factor in carcinogenic among younger patients, it is promotion that facilitates development of a radiation-induced malignancy in older adults.…”
Section: Discussionmentioning
confidence: 99%