Rattus norvegicus
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ABSTRACT:
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:The mammary gland undergoes critical remodeling during pregnancy, making it vulnerable to environmental influences such as antibiotics. This study investigates the long-term effects of prenatal and postnatal exposure to low-dose penicillin (LDP) on immune responses and mammary gland development in mice, along with the potential protective role of the prebiotic AHCC. Pregnant dams were treated with LDP and/or AHCC from late gestation to weaning. Immune markers and blood-milk barrier integrity were assessed in dams, while offspring were evaluated for immune profiles, mammary gland morphology, and epigenetic alterations. LDP exposure triggered inflammation and disrupted DNA methylation in key regulatory genes and microRNAs related to mammary development and the ERK/MAPK pathway. AHCC mitigated these effects, supporting its immunomodulatory and protective potential. These findings highlight the impact of early-life antibiotic exposure on breast tissue development and the possible role of prebiotics in preserving long-term mammary gland homeostasis.
2026-05-01 | GSE296755 | GEO
Project description:Germ-Free critical windows expression data
| PRJEB103022 | ENA
Project description:Environmental exposures across critical developmental windows can significantly influence brain development and contribute to the risk of neurodevelopmental disorders (NDDs). Importantly, emerging clinical evidence suggests that multiple environmental factors during early development result in more pronounced disease phenotypes in offspring. To expand upon this existing notion, we developed a ‘triple-hit’ mouse model to examine the combined effects of maternal social stress, chronic high-fat diet consumption, and early life poly(I:C) exposure on long-term developmental outcomes in offspring. We observed that ‘triple-hit’ male offspring displayed autism-like social deficits and an overall increased susceptibility to NDD-like behavioural alterations in adulthood. Single-cell RNA (scRNA) transcriptomic and bulk proteomic analyses were performed in male triple hit offspring in brain tissue. The results are discussed in the associated publication.
2026-01-19 | PXD060752 | Pride
Project description:Purpose: The high relative biologic effectiveness (RBE) of high-linear energy transfer (LET) heavy-ion radiation has enabled powerful radiotherapy. The potential risk of later onset of secondary cancers, however, has not been adequately studied. We undertook the present study to clarify the RBE of therapeutic carbon ion radiation and molecular changes that occur in the rat mammary cancer model. Methods and materials: We observed 7-8-week-old rats (ACI, F344, Wistar, and Sprague-Dawley) until 1 year of age after irradiation (0.05-2 Gy) with either 290 MeV/u carbon ions with a spread out Bragg peak (LET 40-90 keV/mum) generated from the Heavy-Ion Medical Accelerator in Chiba or (137)Cs gamma-rays. Results: Carbon ions significantly induced mammary carcinomas in Sprague-Dawley rats but less so in other strains. The dose-effect relationship for carcinoma incidence in the Sprague-Dawley rats was concave downward, providing an RBE of 2 at a typical therapeutic dose per fraction. In contrast, approximately 10 should be considered for radiation protection at low doses. Immunohistochemically, 14 of 18 carcinomas were positive for estrogen receptor alpha. All carcinomas examined were free of common H-ras and Tp53 mutations. Importantly, lung metastasis (7%) was characteristic of carbon ion-irradiated rats. Conclusions: We found clear genetic variability in the susceptibility to carbon ion-induced mammary carcinomas. The high RBE for carbon ion radiation further supports the importance of precise dose localization in radiotherapy. Common point mutations in H-ras and Tp53 were not involved in carbon ion induction of rat mammary carcinomas.
2025-04-08 | GSE263550 | GEO
Project description:EFFECT OF POSTNATAL LOW-DOSE EXPOSURE TO ENVIRONMENTAL CHEMICALS ON THE GUT MICROBIOME IN A RODENT MODEL
| PRJEB12306 | ENA