Carcinogenic risks of prenatal ionizing radiation

Brent, Robert L.

doi:10.1016/j.siny.2013.11.009

Cited by 41 publications

(34 citation statements)

References 73 publications

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“…10 Also, cohort studies, which are superior to case-control studies, have not shown increased leukemia risk. 17 The study of childhood leukemias correlated with background radiation 11 does not consider confounding factors such as breastfeeding. Small changes in the results from consideration of such factors could make the increased leukemias statistically insignificant.…”

Section: Rebuttal: Mohan Doss Phdmentioning

confidence: 99%

Point/Counterpoint: Low-dose radiation is beneficial, not harmful

Doss¹,

Little²,

Orton³

2014

Med. Phys.

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Section: Rebuttal: Mohan Doss Phdmentioning

confidence: 99%

Point/Counterpoint: Low-dose radiation is beneficial, not harmful

Doss¹,

Little²,

Orton³

2014

Med. Phys.

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“…The Cancer Genome Atlas project integrated copy number, RNA, methylation status and miRNA data from approximately 300–460 human breast cancer genomes for each breast cancer subtype (9). Breast cancers positive for ER have a distinct methylome profile compared to the more aggressive ER-negative cancers (47). Methylation is a key component of differentiation-associated patterns of transcription in normal development of the mammary gland (48).…”

Section: Discussionmentioning

confidence: 99%

Distinct Luminal-Type Mammary Carcinomas Arise from Orthotopic Trp53-Null Mammary Transplantation of Juvenile versus Adult Mice

et al. 2014

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Age and physiological status, like menopause, are risk factors for breast cancer. Less clear is what factors influence the diversity of breast cancer. In this study, we investigated the effect of host age on the distribution of tumor subtypes in mouse mammary chimera consisting of wild-type hosts and Trp53 nullizygous epithelium, which undergoes a high rate of neoplastic transformation. Wild-type mammary glands cleared of endogenous epithelium at 3 weeks of age were subsequently implanted during puberty (5 weeks) or at maturation (10 weeks) with syngeneic Trp53 null mammary tissue fragments and monitored for 1 year. Tumors arose sooner from adult hosts (AH) compared to juvenile hosts (JH). However, compared to AH tumors, JH tumors grew several times faster, were more perfused, exhibited a 2-fold higher mitotic index and were more highly positive for insulin-like growth factor receptor phosphorylation. Most tumors in each setting were ER positive (80% JH vs 70% AH) but JH tumors were significantly more ER immunoreactive (p=0.0001) than AH tumors. A differential expression signature (JvA) of juvenile versus adult tumors revealed a luminal transcriptional program. Centroids of the human homologs of JvA genes showed that JH tumors were more like luminal A tumors and AH tumors were more like luminal B tumors. Hierarchical clustering with the JvA human ortholog gene list segregated luminal A and luminal B breast cancers across data sets. These data support the notion that age-associated host physiology greatly influences the intrinsic subtype of breast cancer.

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“…Numerous articles using the rat and mouse confirm the all-or-none phenomenon (Job et al 1935;Russell 1950Russell , 1954Hicks et al 1953;Wilson et al 1953b;Russell and Russell 1956;Brent 1960aBrent , 1970Brent , 1999Brent and Bolden 1967a, 1968Coppenger and Brown 1967;Friedberg et al 1973;Schlesinger and Brent 1978;Roux et al 1983;Mazur 1984;Jacquet et al 1995;Adam 2012;Brent 2014b). Many other investigators have confirmed these findings, including Kim et al (2001), indicating no increase in malformations or growth retardation in mice following 2 Gy (gamma rays) at a preimplantation stage.…”

Section: The All-or-none Phenomenonmentioning

confidence: 94%

Protection of the Gametes Embryo/Fetus From Prenatal Radiation Exposure

Brent¹

2015

Health Physics

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There is no convincing evidence of germline mutation manifest as heritable disease in the offspring of humans attributable to ionizing radiation, yet radiation clearly induces mutations in microbes and somatic cells of rodents and humans. Doses to the embryo estimated to be in the range of 0.15-0.2 Gy during the pre-implantation and pre-somite stages may increase the risk of embryonic loss. However, an increased risk of congenital malformations or growth retardation has not been observed in the surviving embryos. These results are primarily derived from mammalian animal studies and are referred to as the "all-or-none phenomenon." The tissue reaction effects of ionizing radiation (previously referred to as deterministic effects) are congenital malformations, mental retardation, decreased intelligence quotient, microcephaly, neurobehavioral effects, convulsive disorders, growth retardation (height and weight), and embryonic and fetal death (miscarriage, stillbirth). All these effects are consistent with having a threshold dose below which there is no increased risk. The risk of cancer in offspring that have been exposed to diagnostic x-ray procedures while in utero has been debated for 55 y. High doses to the embryo or fetus (e.g., >0.5 Gy) increase the risk of cancer. Most pregnant women exposed to x-ray procedures and other forms of ionizing radiation today received doses to the embryo or fetus <0.1 Gy. The risk of cancer in offspring exposed in utero at exposures <0.1 Gy is controversial and has not been fully resolved. Diagnostic imaging procedures using ionizing radiation that are clinically indicated for the pregnant patient and her fetus should be performed because the clinical benefits outweigh the potential oncogenic risks.

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Carcinogenic risks of prenatal ionizing radiation

Cited by 41 publications

References 73 publications

Point/Counterpoint: Low-dose radiation is beneficial, not harmful

Point/Counterpoint: Low-dose radiation is beneficial, not harmful

Distinct Luminal-Type Mammary Carcinomas Arise from Orthotopic Trp53-Null Mammary Transplantation of Juvenile versus Adult Mice

Protection of the Gametes Embryo/Fetus From Prenatal Radiation Exposure

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