Mammary tumors in control rats: Literature tabulation

Sher, Sanford P.

doi:10.1016/0041-008x(72)90285-2

Cited by 15 publications

(3 citation statements)

References 55 publications

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“…Sher (1972) reviewed the frequency of mammary tumours in control rats in studies involving Sprague-Dawley descended female rats including almost 4000 control animals. There were incidence figures ranging from 55-85% in different report with ranges from 19-44% in males.…”

Section: Discussionmentioning

confidence: 99%

Transplacental Carcinogenesis with Radioactive Phosphorus

Berry

Amérigo²,

Nickols

et al. 1983

Human Toxicology

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Section: Discussionmentioning

confidence: 99%

Transplacental Carcinogenesis with Radioactive Phosphorus

Berry

Amérigo²,

Nickols

et al. 1983

Human Toxicology

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“…It is remarkable that tumorigenic effects of these compounds, especially malignant tumor‐inducing potential of 2,7‐diNF, significantly exceeded the level of spontaneous mammary tumor development in Sprague‐Dawley rats. Aging rats of this outbred strain are notorious for a relatively high incidence of mammary tumors, chiefly fibroadenomas 32–35. The data compiled in literature include control groups from numerous carcinogenicity bioassays but the effects of treatment regimens (vehicle, route of administration and duration of treatment) are not discussed.…”

Section: Discussionmentioning

confidence: 99%

Tumorigenicity and genotoxicity of an environmental pollutant 2,7‐dinitrofluorene after systemic administration at a low dose level to female rats

Malejka-Giganti

Parkin

Decker

et al. 2008

Intl Journal of Cancer

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Environmental pollution with nitroaromatic compounds may pose health hazards. We have examined the tumorigenicity in female Sprague-Dawley rats of 2,7-dinitrofluorene (2,7-diNF) and 9-oxo-2,7-diNF administered by intraperitoneal (i.p.) and oral routes at 10 lmol/kg body weight, 3 times per week for 4 weeks. After i.p. treatment, the estimated median latency for the combined malignant and benign mammary tumors was decreased in 2,7-diNF-(p 5 0.003) or 9-oxo-2,7-diNF-treated (p 5 0.007), relative to vehicle-treated rats (42 or 64 vs. 80 weeks, respectively), whereas after oral dosing, there were no significant differences. At 90 weeks, the malignant mammary tumor incidence in 2,7-diNF-, 9-oxo-2,7-diNF-and vehicle-i.p. treated rats was 44 (p 5 0.02 vs. vehicletreated), 25 and 6%, respectively. Liver and mammary gland DNA was analyzed by HPLC combined with electrospray tandem mass spectrometry for the presence of a deoxyguanosine (dG-2,7-diNF) adduct and a deoxyadenosine (dA-2,7-diNF) adduct derived from 2,7-diNF, and a deoxyguanosine (dG-9-oxo-2,7-diNF) adduct derived from 9-oxo-2,7-diNF. Both dG-2,7-diNF and dA-2,7-diNF were detected in DNA of 2,7-diNF-treated rats, whereas only very low levels of dG-9-oxo-2,7-diNF were detected in DNA of 9-oxo-2,7-diNF-treated rats. After i.p. treatment, the dA-2,7-diNF level was higher (p < 0.01) in the mammary gland than liver (13.6 vs. 7.8 adducts/10 8 nucleotides). In the mammary gland, the dG-2,7-diNF level was higher (p < 0.05) after i.p. than oral dosing and also higher (p < 0.05) than in the liver (36 vs. 8.6 and vs. 9.1 adducts/10 8 nucleotides, respectively). The preferential display of carcinogenicity and genotoxicity in the mammary gland by low doses of 2,7-diNF signifies its potential relevance for environmental breast cancer. ' 2008 Wiley-Liss, Inc.Key words: environmental nitroaromatic; rat; mammary cancer; genotoxicity Nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) are widespread environmental pollutants resulting from the incomplete combustion of fossil fuels and atmospheric nitration. [1][2][3] Potential harmful effects of several nitro-PAHs are ascribed to their metabolic activation via nitroreduction to genotoxic species. 4,5 The risks associated with exposure of human populations to mutagenic and carcinogenic nitro-PAHs through inhalation, ingestion or dermal exposure are recognized. 3,[6][7][8][9][10] Nitrofluorenes and their C9-oxidized derivatives constitute a significant fraction of environmental nitro-PAHs. 3,6,7,11,12 2-Nitrofluorene (2-NF) is an abundant compound in diesel, gasoline and kerosene exhausts, and is present in urban air particles at especially high levels (310-5,220 pg/m 3 ) during winter, due to coal and kerosene heating. 6,12 The concentration of 2,7-dinitrofluorene (2,7-diNF; Fig. 1) in the air of Tokyo has been reported to be $30-and $10-fold greater than that of 2-NF and 1-nitropyrene, respectively. 6,13 Administration of 2,7-diNF, 2-NF and 2,5-diNF to female Sprague-Dawley rats at 1.62 mmol/kg of diet for 8 months yielded chi...

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“…The spontaneous incidence of mammary tumors in female rats varies considerably be tween strains; incidences from 10 to 90% have been reported [ 12], In the Sprague-Dawley strain, the spontaneous mammary tumor rate often approaches 50% of female rats dur ing their life span, with tumors generally oc curring during the second year of life [12,13]. In the present study, about two thirds (16/25) of rats aged from 1 to 2 Vi years developed tumors, whereas only a few younger females developed tumors during the observation time.…”

Section: Discussionmentioning

confidence: 99%

Aryl Hydrocarbon Hydroxylase Activity in Spontaneous Mammary Tumors in Rat

Pyykkö

Jaakkola²,

Söderström³

et al. 1994

Tumor Biol

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The development of spontaneous mammary tumors was observed for about 2 years in a group of 25 female Sprague-Daw-ley rats aged over 1 year at the beginning of the study. All younger females in our animal facility were similarly monitored. In old females, the incidence of spontaneous mammary tumors was 64%. The parity of rats did not protect them from tumorigenesis, but the proportion of malignant tumors was higher in virgin (57%) than in parous (13%) rats. Activities of cytochrome P450IAI -dependent enzyme (aryl hydrocarbon hydroxylase, AHH) and NADPH-cytochrome P450 reductase (NCR) were determined in microsome fractions isolated from livers, lungs, uteri and tumors of rats. AHH and NCR activities in tumors and uteri were low compared to those in livers or lungs. In tumors, the activity distributions were wide, even in different tumors of the same animal the AHH activities varied as widely as between different animals. The activities in benign and malignant tumors were not statistically significantly different. No correlation with liver, lung or uterine activities was found either. With ageing of the rat, the AHH activities in tumors, liver and lungs decreased. The behavior of AHH in spontaneous mammary tumors in rats seems to be similar to that found in chemically induced tumors and seems to show individual regulation, possibly altered by tumorigenesis in each individual tumor.

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Mammary tumors in control rats: Literature tabulation

Cited by 15 publications

References 55 publications

Transplacental Carcinogenesis with Radioactive Phosphorus

Transplacental Carcinogenesis with Radioactive Phosphorus

Tumorigenicity and genotoxicity of an environmental pollutant 2,7‐dinitrofluorene after systemic administration at a low dose level to female rats

Aryl Hydrocarbon Hydroxylase Activity in Spontaneous Mammary Tumors in Rat

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