Cancer Incidence in Atomic Bomb Survivors. Part III: Leukemia, Lymphoma and Multiple Myeloma, 1950-1987

Preston, Dale L.; Kusumi, Shizuyo; Tomonaga, Masao; Izumi, Shizue; Ron, Elaine; Kuramoto, Atsushi; Kamada, Nanao; Dohy, Hiroo; T, Matsui; Nonaka, Hiroaki; Thompson, Desmond; Soda, Midori; Mabuchi, Kiyóhiko

doi:10.2307/3578893

Cited by 697 publications

(487 citation statements)

References 23 publications

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“…Experimental data as well as cancer incidence records of atomic bomb survivors indicated that BCR/ABL translocation might occur after irradiation (Preston et al, 1994;Deininger et al, 1998).…”

Section: Generation Of Dsbsmentioning

confidence: 99%

Fusion tyrosine kinases: a result and cause of genomic instability

Penserga

Skórski

2006

Oncogene

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Section: Generation Of Dsbsmentioning

confidence: 99%

Fusion tyrosine kinases: a result and cause of genomic instability

Penserga

Skórski

2006

Oncogene

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“…The only established causal exposure for childhood leukemia is ionizing radiation. This unambiguous conclusion is derived from data on Japanese atomic bomb survivors from 1945 who were acutely exposed to up to 4200 mSv 43 and, at a much lower dose level (B10 mSv), from historical data on diagnostic exposure of the fetus from X-ray pelvimetry during pregnancy. 44 Unfortunately, most of these environmental exposures lack a biological rationale or consistent epidemiological evidence.…”

Section: Environmental Exposures and Delayed Infection Early In Life mentioning

confidence: 99%

Insights into the cellular origin and etiology of the infant pro-B acute lymphoblastic leukemia with MLL-AF4 rearrangement

et al. 2010

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Infant acute lymphoblastic leukemia (ALL) involving mixedlineage leukemia (MLL) fusions has attracted a huge interest in basic and clinical research because of its prenatal origin, mixed-lineage phenotype, dismal prognosis and extremely short latency. Over 90% of infant ALLs are pro-B ALL harboring the leukemic fusion MLL-AF4. Despite the fact that major achievements have provided a better understanding about the etiology of infant MLL-AF4 þ ALL over the last two decades, key questions remain unanswered. Epidemiological and genetic studies suggest that the in utero origin of MLL rearrangements in infant leukemia may be the result of prenatal exposure to genotoxic compounds. In fact, chronic exposure of human embryonic stem cells (hESCs) to etoposide induces MLL rearrangements and makes hESC more prone to acquire subsequent chromosomal abnormalities than postnatal CD34 þ cells, linking embryonic exposure to topoisomerase II inhibitors to genomic instability and MLL rearrangements. Unfortunately, very little is known about the nature of the target cell for transformation. Neuron-glial antigen 2 expression was initially claimed to be specifically associated with MLL rearrangements and was recently shown to be readily expressed in CD34 þ CD38 þ , but not CD34 þ CD38À cells suggesting that progenitors rather than stem cells may be the target cell for transformation. Importantly, the recent findings showing that MLL-AF4 rearrangement is present and expressed in mesenchymal stem cells from infant patients with MLLAF4 þ ALL challenged our current view of the etiology and cellular origin of this leukemia. It becomes therefore crucial to determine where the leukemia relapses come from and how the tumorstroma relationship is defined at the molecular level. Finally, MLL-AF4 leukemogenesis has been particularly difficult to model and bona fide MLL-AF4 disease models do not exist so far. It is likely that the current disease models are missing some essential ingredients of leukemogenesis in the human embryo/ fetus. We thus propose modeling MLL-AF4 þ infant pro-B ALL using prenatal hESCs.

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“…Some A-bomb survivor studies were inconclusive regarding a relationship between radiation dose and MM, while others indicated a close association between them (Mancuso et al, 1977;Gilbert & Marks, 1979;Huntington et al, 1979;Cuzick, 1981;Gilbert et al, 1993). While Ichimaru et al (1982) reported a significant increase in MM incidence among A-bomb survivors in the period 1950-1976, a 1950-1990 incidence study that used new criteria showed no association of MM with radiation dose (Preston et al, 1994). A mortality study during the same period showed a significant increase in MM incidence among A-bomb survivors (Pierce et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Monoclonal gammopathy of undetermined significance in atomic bomb survivors: incidence and transformation to multiple myeloma

2003

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Summary. Among 6737 atomic bomb survivors who did not have monoclonal gammopathy at the first examination, 112 developed monoclonal gammopathy of undetermined significance (MGUS) between 1985 and 2001. The crude incidence rate was 164 per 100 000 person-years in the overall study population, with a sharp increase in incidence after age 60 years. The incidence was not significantly associated with radiation dose (P ¼ 0AE91), although the incidence at less than 80 years of age showed a marginally significant association (P ¼ 0AE05). Among 75 patients with MGUS detected in 1985, 50 patients (67%) had died by 2001, 16 (21%) of these deaths were due to multiple myeloma (MM). MM mortality among MGUS patients was 2284 per 100 000 person-years while the rate in the total population was 14AE6 per 100 000 person-years. The risk of MM mortality was greater in the older generation. The transformation from MGUS to MM was faster in exposed persons than in non-exposed persons, but this was not statistically significant.

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Cancer Incidence in Atomic Bomb Survivors. Part III: Leukemia, Lymphoma and Multiple Myeloma, 1950-1987

Cited by 697 publications

References 23 publications

Fusion tyrosine kinases: a result and cause of genomic instability

Fusion tyrosine kinases: a result and cause of genomic instability

Insights into the cellular origin and etiology of the infant pro-B acute lymphoblastic leukemia with MLL-AF4 rearrangement

Monoclonal gammopathy of undetermined significance in atomic bomb survivors: incidence and transformation to multiple myeloma

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