Actuarial analysis of the hazard for mammary carcinogenesis in different rat strains after X- and neutron irradiation

Broerse, J.J.; Hennen, L.A.; Solleveld, Henk A.

doi:10.1016/0145-2126(86)90291-2

Cited by 20 publications

(13 citation statements)

References 4 publications

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“…Since the demonstration in the early 1950s that a single supralethal dose of x-rays to female Holtzman rats (a S-D stock) maintained by temporary parabiosis induced an increased number of benign and malignant mammary tumors within 6 months [63], numerous investigations of radiation-induced mammary tumorigenesis in the rat have been carried out. Sublethal doses of different types of radiation, including x-rays and neutrons, were shown to induce mammary tumor development, often within a year, with linear dose-effect relationships for neutrons over the total dose range and for x-rays down to dose levels of 0.2 Gy [64,65]. Irradiation of animals with fractionated doses of It-radiation has resulted in linear-quadratic dose-response curves [66].…”

Section: Radiation-induced Mammary Tumorigenesismentioning

confidence: 98%

Experimentally induced mammary tumors in rats

Russo

1996

Breast Cancer Res Tr

231

170

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Among the multiple experimental animal models employed for analyzing the various aspects of mammary carcinogenesis, the induction of mammary tumors in rats by chemical carcinogens is one of the models most utilized. Experimentally-induced mammary tumors in rodents have proven to constitute useful tools for the study of the pathogenesis of cancer and of the molecular mechanisms involved in the initiation and progression of the neoplastic process. In vivo experimental animal models provide information not available in human populations; they are adequate for hazard identification, dose-response modeling, exposure assessment, and risk characterization, the four required steps for quantifying the estimated risk of cancer development associated with toxic chemical exposure. Using the DMBA rat mammary model, we have been able to demonstrate that the carcinogen acts on the intermediate cell of the terminal end bud (TEB), and that this structure is the one that evolves to intraductal proliferation, carcinoma in situ, and invasive carcinoma. There are several factors that regulate the susceptibility of the TEB; some of them are: a) topographic location of the mammary gland, b) age of the animal, and c) reproductive history. The understanding of the mechanisms that modulate tumorigenesis will further our knowledge and understanding in the prevention of the disease, as a result of the development of strategies for stopping the progression of the initiated cells.

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Section: Radiation-induced Mammary Tumorigenesismentioning

confidence: 98%

Experimentally induced mammary tumors in rats

Russo

1996

Breast Cancer Res Tr

231

170

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“…In addition to lifestage differences in susceptibility to radiation-induced cancer, tumor response to radiation in adult animals varies depending on strain (Broerse et al 1986), hormone status (i.e., estrogen levels; Bartstra et al 2000), and whether the dose of radiation is a single or fractionated exposure (Maisin et al 1988). There are many reasons that fetuses, infants, and children are more sensitive to chemicals than are adults.…”

Section: Health Decisions Must Address Interindividual Differences Inmentioning

confidence: 99%

Fundamental Flaws of Hormesis for Public Health Decisions

Thayer

Melnick

Burns³

et al. 2005

Environ Health Perspect

109

120

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Hormesis (defined operationally as low-dose stimulation, high-dose inhibition) is often used to promote the notion that while high-level exposures to toxic chemicals could be detrimental to human health, low-level exposures would be beneficial. Some proponents claim hormesis is an adaptive, generalizable phenomenon and argue that the default assumption for risk assessments should be that toxic chemicals induce stimulatory (i.e., “beneficial”) effects at low exposures. In many cases, nonmonotonic dose–response curves are called hormetic responses even in the absence of any mechanistic characterization of that response. Use of the term “hormesis,” with its associated descriptors, distracts from the broader and more important questions regarding the frequency and interpretation of nonmonotonic dose responses in biological systems. A better understanding of the biological basis and consequences of nonmonotonic dose–response curves is warranted for evaluating human health risks. The assumption that hormesis is generally adaptive is an oversimplification of complex biological processes. Even if certain low-dose effects were sometimes considered beneficial, this should not influence regulatory decisions to allow increased environmental exposures to toxic and carcinogenic agents, given factors such as interindividual differences in susceptibility and multiplicity in exposures. In this commentary we evaluate the hormesis hypothesis and potential adverse consequences of incorporating low-dose beneficial effects into public health decisions.

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“…The administration of DMBA to virgin rats of different 50 51 f,Og 67 (26) 77 (26) 77 (26) 60 (26) 40 (24) 36 (24) 19 (24) 0 (24) 74 (24) 79 (24) 42 (24) 24 (24) 33 (26) 80 (26) 34 (26) 88 (26) 100 (26) 70 (26) :11 (26) 59 (26) 20 (26) 66 (22) 87 (22) 63 (22) 87 (22) 100 (22) 94 (22) 59 (22) 30 (22) 22 (22) 0 (22) Percentage by weight in purified diets; if value not given, rats were fed natural ingredient diets that contain, generally. 4 to 5% fat.…”

Section: Experimentally-induced Mammary Tumors In Rats Chemically -Inmentioning

confidence: 99%