Mammary Carcinogenesis in Different Rat Strains after Irradiation and Hormone Administration

Broerse, J.J.; Hennen, L.A.; Klapwijk, Wim M.; Solleveld, Henk A.

doi:10.1080/09553008714551381

Cited by 26 publications

(20 citation statements)

References 12 publications

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“…Radiation and estrogens, namely 17~-estradiol (E2) or DES, were reported to exert either an additive [72] or a synergistic effect [73,74]. The effect of E 2 administration and irradiation on mammary tumorigenesis is equal for hormone administration 1 week before, or beginning 12 weeks after irradiation [72]. This additive effect of hormone administration and irradiation was not evident if the hormone was administered beginning 24 weeks after irradiation.…”

Section: Rat Mammary Tumors 11mentioning

confidence: 94%

“…The latency period for tumor development is shortened considerably in estrogen-treated rats; there is an increase in the number of rats with carcinomas, especially cribriform carcinomas [18], and in the number of tumors/tumor-bearing rat [71]. Radiation and estrogens, namely 17~-estradiol (E2) or DES, were reported to exert either an additive [72] or a synergistic effect [73,74]. The effect of E 2 administration and irradiation on mammary tumorigenesis is equal for hormone administration 1 week before, or beginning 12 weeks after irradiation [72].…”

Section: Rat Mammary Tumors 11mentioning

confidence: 98%

“…The fractions have been delivered in a variety of different protocols, for example, at 12-hour intervals for 60 days [66], semi-weekly for up to 16 weeks [69], and monthly for up to 10 months [70]. In general, no increase in tumor latency, incidence, or total number of mammary tumors was found, compared with animals receiving an equivalent amount of radiation given as a single dose.…”

Section: Radiation-induced Mammary Tumorigenesismentioning

confidence: 99%

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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: Rat Mammary Tumors 11mentioning

confidence: 94%

Section: Rat Mammary Tumors 11mentioning

confidence: 98%

Section: Radiation-induced Mammary Tumorigenesismentioning

confidence: 99%

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Experimentally induced mammary tumors in rats

Russo

1996

Breast Cancer Res Tr

231

170

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“…In addition to epilepsy research, WAG rats are widely used in cancer research, including studies on gamma irradiation on induction of mammary carcinoma [49, 50]. …”

Section: Discussionmentioning

confidence: 99%

Power Frequency Magnetic Fields Increase Cell Proliferation in the Mammary Gland of Female Fischer 344 Rats but Not Various Other Rat Strains or Substrains

Fedrowitz

Löscher²

2005

Oncology

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Epidemiological data have raised concerns about the relationship between exposure to power frequency magnetic fields (MFs) and breast cancer. We have shown previously that 50-Hz MFs at microtesla flux densities enhance mammary gland tumor development and growth in the 7,12-dimethylbenz[a]anthracene (DMBA) model of breast cancer in female Sprague-Dawley (SD) rats. We also demonstrated that MF exposure results in an enhanced proliferative activity of the mammary epithelium of SD rats, which is a likely explanation for the cocarcinogenic or tumor-promoting effects of MF exposure in the DMBA model. Comparison of different SD substrains indicated that the genetic background plays a pivotal role in these effects of MF exposure. This prompted us to compare the effects of MF exposure (100 µT, 2 weeks) on cell proliferation in the mammary gland in eight different strains and substrains of outbred and inbred rats. Proliferation of epithelial cells in the mammary tissue and adjacent skin was examined by labeling proliferating cells with bromodeoxyuridine (BrdU). In addition to the MF-sensitive SD substrain (SD1) previously used in our experiments, Fischer 344 rats were the only strain in which MF exposure significantly enhanced BrdU labeling in the mammary epithelium, indicating a marked increase in cell proliferation. The MF-induced increase in BrdU labeling in Fischer 344 rats was similar to that seen after DMBA application. Furthermore, whole mount analysis of mammary tissue from Fischer 344 rats demonstrated that MF exposure increased the number of terminal end buds, i.e. the site of origin of mammary carcinomas. By comparison with MF-insensitive inbred rat strains, Fischer 344 rats may serve to evaluate the genetic factors underlying sensitivity to cocarcinogenic or tumor-promoting effects of MF exposure.

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“…Studies on mammary tumourigenesis, performed at TNO in three rat strains, notably Sprague-Dawley, WAG/Rij and BN/BiRij, have shown that only in WAG/Rij rats was an appreciable number of carcinomas induced by irradiation ( . Earlier analysis of the TNO results (Broerse et al 1983) was based on the excess actuarial incidence at an age of 22 months or on the forward shift in time. For the incidence of fibroadenomas in WAG/Rij rats, the exponent of the dose-effect curve for excess actuarial incidence after irradiation with 0-5 MeV neutrons was also lower than 1.…”

Section: Nature Of Dose-response Relationshipsmentioning

confidence: 99%

Radiation Carcinogenesis in Experimental Animals and Its Implications for Radiation Protection

Broerse

Hennen²,

Zwieten

1985

International Journal of Radiation Biology and Related Studies

Self Cite

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Cancer induction is generally considered to be the most important somatic effect of low doses of ionizing radiation. It is therefore of great concern to assess the quantitative cancer risk of exposure to radiations of different quality and to obtain information on the dose-response relationships for carcinogenesis. Tissues in the human with a high sensitivity for cancer induction include the bone marrow, the lung, the thyroid and the breast in women. If the revised dosimetry estimates for the Japanese survivors of the atomic bomb explosions are correct, there is no useful data base left to derive r.b.e. values for human carcinogenesis. As a consequence, it will be necessary to rely on results obtained in biological systems, including experimental animals, for these estimates. With respect to radiation protection, the following aspects of experimental studies on radiation carcinogenesis are of relevance: Assessment of the nature of dose-response relationships. Determination of the relative biological effectiveness of radiations of different quality. Effects of fractionation or protraction of the dose on tumour development. For the analysis of tumour data in animals, specific approaches have to be applied which correct for competing risks. These methods include actuarial estimates, non-parametric models and analytical models. The dose-response curves for radiation-induced cancers in different tissues vary in shape. This is exemplified by studies on myeloid leukaemia in mice and mammary neoplasms in different rat strains. The results on radiation carcinogenesis in animal models clearly indicate that the highest r.b.e. values are observed for neutrons with energies between 0.5 and 1 MeV. On the basis of such results it might be concluded that the maximum quality factor of 10 for neutrons should be increased. Based on current evidence, an increase by a factor of 2 to 3 seems more realistic than a tenfold rise. The diversity of dose-response relationships point to different mechanisms involved in the induction of different tumours in various species and even in different strains of the same species.

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Mammary Carcinogenesis in Different Rat Strains after Irradiation and Hormone Administration

Cited by 26 publications

References 12 publications

Experimentally induced mammary tumors in rats

Experimentally induced mammary tumors in rats

Power Frequency Magnetic Fields Increase Cell Proliferation in the Mammary Gland of Female Fischer 344 Rats but Not Various Other Rat Strains or Substrains

Radiation Carcinogenesis in Experimental Animals and Its Implications for Radiation Protection

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