Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA191783 | ENA |
REPOSITORIES: ENA
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Project description:Comparison of radiation-induced rat mammary carcinomas from individuals with different sensitivity to diet-induced obesity
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Project description:Global DNA methylation profiling of radiation-induced rat mammary carcinomas
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Project description:Radiation-specific DNA copy number aberration in rat mammary carcinoma.
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Project description:Real-time quantitative PCR analysis of male rat fed either Lard based or Corn Oil based high fat diet and their female offspring
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Project description:Although various mechanisms have been inferred for combinatorial actions of multiple carcinogens, these mechanisms have not been well demonstrated in experimental carcinogenesis models. We evaluated mammary carcinogenesis initiated by combined exposure to various doses of radiation and chemical carcinogens. Female rats at 7 weeks of age were M-NM-3-irradiated (0.2M-bM-^@M-^S2 Gy) and/or exposed to 1-methyl-1-nitrosourea (20 or 40 mg/kg, single intraperitoneal injection) or 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (40 mg/kg/day by gavage for 10 days) and were observed until 50 weeks of age. The incidence of mammary carcinoma increased steadily as a function of radiation dose in the absence of chemicals; mathematical analysis supported an additive increase when radiation was combined with a chemical carcinogen, irrespective of the chemical species and its dose. Hras mutations were characteristic of carcinomas that developed after chemical carcinogen treatments and were overrepresented in carcinomas induced by the combination of radiation and MNU (but not PhIP), indicating an interaction of radiation and MNU at the level of initiation. The expression profiles of seven classifier genes, previously shown to distinguish two classes of rat mammary carcinomas, categorized almost all examined carcinomas that developed after individual or combined treatments with radiation (1 Gy) and chemicals as belonging to a single class; more comprehensive screening using microarrays and a separate test sample set failed to identify differences in gene expression profiles among these carcinomas. These results suggest that a complex, multilevel interaction underlies the combinatorial action of radiation and chemical carcinogens in the experimental model. Mammary cancers were from untreated rats (n = 3) and rats treated with radiation (1 Gy; n = 4), MNU (40 mg/kg; H-rasM-bM-^@M-^Smutated cancers, n = 5; H-rasM-bM-^@M-^Snonmutated cancers, n = 4), PhIP (H-rasM-bM-^@M-^Smutated, n = 1; H-rasM-bM-^@M-^Snonmutated, n = 3), radiation 1 Gy plus MNU (40 mg/kg; H-rasM-bM-^@M-^Smutated, n = 5; H-rasM-bM-^@M-^Snonmutated, n = 4) and radiation 1 Gy plus PhIP (H-rasM-bM-^@M-^Snonmutated , n = 4). Normal mammary tissues were from untreated rats (n = 3).
2013-08-29 | E-GEOD-44786 | biostudies-arrayexpress
Project description:Influence of intrauterine low protein diet on ductal morphogenesis of the rat mammary gland.
| PRJNA150087 | ENA
Project description:Aberrant expression of microRNAs (miRNAs) is frequently associated with a variety of cancers, including breast cancer. We and others have demonstrated that radiation-induced rat mammary cancer exhibits a characteristic gene expression profile and a random increase in aberrant DNA copy number; however, the role of aberrant miRNA expression is unclear. We performed a microarray analysis of frozen samples of eight mammary cancers induced by gamma-irradiation (2 Gy), eight spontaneous mammary cancers, and seven normal mammary samples. We found that a small set of miRNAs was characteristically overexpressed in radiation-induced cancer. Quantitative RT-PCR analysis confirmed that miR-135b, miR-192, miR-194, and miR-211 were significantly upregulated in radiation-induced mammary cancer compared with spontaneous cancer and normal mammary tissue. The expression of miR-192 and miR-194 also was upregulated in human breast cancer cell lines compared with non-cancer cells. Manipulation of the miR-194 expression level using a synthetic inhibiting RNA produced a small but significant suppression of cell proliferation and upregulation in the expression of several genes that are suggested to act as tumor suppressors in MCF-7 and T47D breast cancer cells. Thus, the induction of rat mammary cancer by radiation involves aberrant expression of miRNAs, which may favor cell proliferation. We performed miRNA microarray analysis on mammary carcinomas in Sprague-Dawley rat to identify radiation-specific miRNA expression patterns compared with spontaneous mammary carcinomas and normal mammary tissues.
2013-01-07 | E-GEOD-34119 | biostudies-arrayexpress