Rattus norvegicus
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PROVIDER: PRJNA293572 | ENA |
REPOSITORIES: ENA
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Project description:Exposure to common environmental chemicals, including those found in personal care products has been linked to mammary cancer at high doses in animal models. Their effects at low doses at levels comparable to human exposure, especially during critical windows of development remain poorly understood. Using a Sprague-Dawley rat model, we investigated the effects of of three environmental chemicals – diethyl phthalate (DEP), methyl paraben (MPB) and triclosan (TCS) – on the transcriptome of normal developing mammary glands at low doses mimicking human exposure. Rats were exposed during three windows of early development – perinatal (gestation day (GD) 1 - 20 or postnatal day (PND) 1 - 20), prepubertal (PND 21 - 41) and pubertal (PND 42 - 62), as well as chronic exposure from birth to end of lactation (PND 1 - 146). Mammary gland whole-transcriptomes were profiled by Affymetrix rat gene 2.0 st arrays.
2016-10-19 | GSE72276 | GEO
Project description:Mammary transcriptome of rats treated with low-dose environmental chemicals from birth to adulthood
| PRJNA377433 | ENA
Project description:Exposure to common environmental chemicals, including those found in personal care products has been linked to mammary cancer at high doses in animal models. Their effects at low doses at levels comparable to human exposure remain poorly understood. Using a Sprague-Dawley rat model, we investigated the effects of three prevalently used environmental chemicals – diethyl phthalate (DEP), methyl paraben (MPB), triclosan (TCS) – and their mixture (MIX) on the transcriptome of normal developing mammary at levels mimicking human exposure. Rats were exposed from birth to adulthood in parous and nulliparous settings. We used affymetrix arrays to assess the influence of diethyl phthalate (DEP), methyl paraben (MPB), triclosan (TCS) and their mixture (MIX) on global gene expression profiles in rat mammary tissues, using doses comparable to human exposure. Exposure was from birth to adulthood (postnatal day 1 – 180) in parous and nulliparous rats.
2020-04-28 | GSE95554 | GEO
Project description:Environmental chemicals such as bisphenol A (BPA) are thought to contribute to carcinogenesis through their endocrine-disrupting effects. However BPA replacement chemicals are structurally similar, and little data exist describing their effects on the human body and environment. We established non-malignant human mammary organoid cultures to investigate the effects of BPA replacement chemicals on organoid morphology and protein abundance. At low-nanomolar doses, replacement chemicals, in particular BPS, induced branching and disrupted the organized mammary organoid architecture. BPS exposure likely alters mammary cell-type proportions and induces branching of predominately myoepithelial cells. Treatment with different replacement chemicals resulted in distinct proteomic changes. BPS exposure induced Cdc42-interacting protein 4 (CIP4), a protein known to support invadopodia formation and mesenchymal phenotypes. Our study provides evidence that replacement bisphenols have pro-tumorigenic effects on mammary morphology and the proteome, highlighting the necessity of comprehensive studies to evaluate the potential harm of replacement chemicals.
2021-06-11 | MSV000087617 | MassIVE
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:Diethlstilbestrol (DES) is a synthetic estrogen prescribed to several millions of pregnant women worldwide. The risk for breast cancer after age 40 in women prenatally exposed to DES has been reported, however, the precise mechanism of susceptibilities to breast cancer remains to be resolved. To understand the mechanism of effect of intrauterine exposure to DES on human mammary glands at peripubertal stage, we investigated the global gene expression profile of terminal end buds (TEBs), the target of carcinogen, in rat mammary glamds at postnatal days (PND) 35 and 49, equivalent to peripubertal stage in human, exposed to low or high dose of DES at neonatal period. In all group, the number of TEBs was gradually increased and peaked at PND35 and decreased at PND49. At PND 35 and 49, low dose of DES-treated group showed highest number of TEBs. At PND35, β- and γ-casein mRNA expression inreased 8.19-fold and 26.05-fold, respectively, and the most significant network revealed by IPA analyses showed relevance of NF-κB in low dose of DES-treated group. The present findings suggested that deregulation of mammary gland differentiation and development-related genes group may contribute to the increase of number of TEBs at critical period of carcinogen susceptibilities. Experiment: We used laser capture microdissection to specifically isolate the cells from terminal end buds (TEBs) in rat mammary gland at 35 and 49 days after birth. Inbred Sprague-Dawley female rats were subcutaneously given 0.05ml sesame oil (group I, control) and either 1 μg (group II) or 100 μg (group III) diethlstilbestrol (DES, Sigma Chemical Co., St. Louis, Mo. USA) dissolved in 0.05 ml sesame oil within 24 hr of birth. Animal were weaned at 21 days of birth and each group of rats was autopsied at 35 and 49 days of birth. From group I (35 days of birth: n=2, 49 days of birth: n=2), group II (35 days of birth: n=2, 49 days of birth: n=2), group III (35 days of birth: n=2, 49 days of birth: n=2), we performed a hybridization, respectively.
2010-11-06 | E-GEOD-25043 | biostudies-arrayexpress
Project description:EFFECT OF POSTNATAL LOW-DOSE EXPOSURE TO ENVIRONMENTAL CHEMICALS ON THE GUT MICROBIOME IN A RODENT MODEL
| PRJEB12306 | ENA
Project description:Syracuse High/Low Avoidance Learning in Rats
| PRJNA87963 | ENA
Project description:Some previous experimental studies have shown that early in life intake of high-fat or Western-style diets did alter the development of mammary cancer in adulthood female rats. Thus, the present study investigated the distinct gene expression patterns of chemically induced mammary tumors derived from female offspring whose dams intake control diet (CD) or Western-style diet (WD). During gestational days (GD) 12-21 and post-natal days (PND) 1-21, pregnant Sprague-Dawley (SD) rats were fed a CD diet or WD (high-fat and low-fiber and oligoelements) diet. On postnatal day (PND) 21, the female offspring received a single dose of carcinogen N-Methyl-N-Nitrosourea (MNU, 50 mg/kg) and CD diet for 12 weeks. Latency, incidence and tumor burden were registered. Mammary tumors samples were collected and histopathology and gene expression analysis were performed.
2018-10-12 | GSE96520 | GEO
Project description:Methylmercury is a bioaccumulated environmental neurotoxicant, however, it remains largely unknown regarding impacts of non-apoptotic low dose methylmercury on embryonic cerebral cortex development. Here, using single cell RNA-seq analysis we show that prenatal exposure of MeHg favors RGP developmental trajectory towards directly producing cortical neurons, omitting intermediate progenitor stage. Our findings reveal the outcomes of low dose MeHg exposure on the fetal brain development and provide insights into its underlying mechanisms and potential therapeutic strategy.
2023-02-13 | GSE178929 | GEO