Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA96791 | ENA |
REPOSITORIES: ENA
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Project description:Aged male Fischer 344/N rats are prone to developing spontaneous peritoneal mesotheliomas, which arise predominantly from the tunica vaginalis of the testes. A definitive cause for the predominance of this neoplasm in F344/N rats is unknown. Investigation of the molecular alterations that occur in spontaneous rat mesotheliomas may provide insight into their pathogenesis, as well enable a better understanding regarding the mechanisms underlying chemically induced mesothelioma in rodents. Mesothelial cell function represents a complex interplay of pathways related to host defense mechanisms and maintenance of cellular homeostasis. Global gene expression profiles of spontaneous mesotheliomas from vehicle control male F344/N rats from two-year National Toxicology Program carcinogenicity bioassays were analyzed to determine the molecular features of these tumors, and elucidate tumor-specific gene expression profiles. The resulting gene expression pattern showed that spontaneous mesotheliomas are associated with upregulation various growth factors, oncogenes, cytokines, pattern recognition response receptors (PRR) and pathogen associated molecular patterns (PAMP) receptors, and the production of reactive oxygen and nitrogen species, as well as downregulation of apoptosis pathways. Alterations in these pathways in turn trigger molecular responses that stimulate cell proliferation and promote tumor survival and progression. Five spontaneous malignant mesotheliomas from two-year-old F344/N rats and six normal Fred-PE mesothelial cell culture samples (as controls).
2013-09-06 | E-GEOD-47581 | biostudies-arrayexpress
Project description:This study was performed to characterize the gene expression profile of rat peritoneal mesothelioma (RPM) formation following treatment of Fischer 344 rats with o-nitrotoluene (o-NT) or bromochloracetic acid (BCA). Keywords: Rat, Mesotheliomas, Bromochloractetic acid, o-Nitrotoluene, Carcinogenesis, Microarray
2006-04-20 | GSE4682 | GEO
Project description:Ventral prostate in male F344 rats: Control vs. PhIP treatment
| PRJNA376424 | ENA
Project description:A recent two-year NTP cancer bioassay showed a marked increase in the incidence of malignant mesothelioma arising from the tunica vaginalis in male Fischer 344/N rats exposed to Vinylidene chloride (VDC). Aged male F344/N rats are prone to developing spontaneous peritoneal mesotheliomas, which also arise predominantly from the tunica vaginalis of the testes. A definitive mechanism for the observed increased incidence in VDC-exposed rats is unknown. Investigation of the molecular alterations that occur in mesotheliomas from vehicle control and VDC-exposed rats may provide insight into their pathogenesis, as well enable a better understanding regarding the mechanisms underlying chemically induced mesothelioma in rodents. Mesothelial cell function represents a complex interplay of pathways related to host defense mechanisms and maintenance of cellular homeostasis. Global gene expression profiles of spontaneous mesotheliomas from vehicle control male F344/N rats from various two-year National Toxicology Program carcinogenicity bioassays were compared to mesotheliomas from VDC-exposed rats to characterize the molecular features that are present in mesotheliomas from VDC-exposed animals, and to elucidate tumor-specific gene expression profiles. The resulting gene expression pattern showed that mesotheliomas from VDC-exposed animals are genomically very different from spontaneous tumors; while both tumor types are characterized by alterations in gene expression associated with carcinogenic pathways (oncogenes, tumor suppressor genes, growth factors, etc.), mesotheliomas from VDC-exposed animals are associated with increased dysreguation of immune pathways and inflammatory mediators. Alterations in these pathways may suggest a pro-inflammatory and immune dysfunction signature as one mechanism in the observed increased incidence of these tumors in VDC-exposed animals.
2013-09-06 | GSE47581 | GEO
Project description:Toxicogenomic Assessment of Liver Responses following subchronic exposure to furan in Fischer F344 rats [miRNA]
| PRJNA265191 | ENA
Project description:Toxicogenomic Assessment of Liver Responses following subchronic exposure to furan in Fischer F344 rats [cRNA]
| PRJNA265190 | ENA
Project description:Gene expression profiles in liver of F344 rat treated with chemical
| PRJNA195581 | ENA
Project description:Gene expression analysis of liver and kidney following methapyrilene treatment in male Sprague-Dawley rats
| PRJNA96287 | ENA
Project description:Malignant mesothelioma is an aggressive cancer that often originates in the pleural and peritoneal mesothelium. Exposure to asbestos is a frequent cause. But studies in rodents showed that certain multiwalled carbon nanotubes (MWCNTs) can induce malignant mesotheliomas. This study aimed to understand molecular pathways leading to the development of malignant mesotheliomas induced by MWCNTs and amosite asbestos in Wistar rats. Using Affymetrix microarrays, we carried out genome-wide transcriptome analysis on malignant peritoneal meosotheliomas induced by MWCNTs and amosite asbestos. The transcriptome of MWCNTs and amosite asbestos-induced mesotheliomas exhibited commonalities, but also differences pertaining to differentially-expressed genes (DEGs), regulated canonical pathways, and molecular functions.
2024-02-01 | GSE233803 | GEO
Project description:A series of two color gene expression profiles obtained using Agilent 44K expression microarrays was used to examine sex-dependent and growth hormone-dependent differences in gene expression in rat liver. This series is comprised of pools of RNA prepared from untreated male and female rat liver, hypophysectomized (‘Hypox’) male and female rat liver, and from livers of Hypox male rats treated with either a single injection of growth hormone and then killed 30, 60, or 90 min later, or from livers of Hypox male rats treated with two growth hormone injections spaced 3 or 4 hr apart and killed 30 min after the second injection. The pools were paired to generate the following 6 direct microarray comparisons: 1) untreated male liver vs. untreated female liver; 2) Hypox male liver vs. untreated male liver; 3) Hypox female liver vs. untreated female liver; 4) Hypox male liver vs. Hypox female liver; 5) Hypox male liver + 1 growth hormone injection vs. Hypox male liver; and 6) Hypox male liver + 2 growth hormone injections vs. Hypox male liver. A comparison of untreated male liver and untreated female liver liver gene expression profiles showed that of the genes that showed significant expression differences in at least one of the 6 data sets, 25% were sex-specific. Moreover, sex specificity was lost for 88% of the male-specific genes and 94% of the female-specific genes following hypophysectomy. 25-31% of the sex-specific genes whose expression is altered by hypophysectomy responded to short-term growth hormone treatment in hypox male liver. 18-19% of the sex-specific genes whose expression decreased following hypophysectomy were up-regulated after either one or two growth hormone injections. Finally, growth hormone suppressed 24-36% of the sex-specific genes whose expression was up-regulated following hypophysectomy, indicating that growth hormone acts via both positive and negative regulatory mechanisms to establish and maintain the sex specificity of liver gene expression. For full details, see V. Wauthier and D.J. Waxman, Molecular Endocrinology (2008)
2008-05-24 | GSE11529 | GEO