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Alterations in hepatic gene expression induced by chromic exposure to high levels of the SV40 LT/st oncoproteins (4P)

ABSTRACT: Hepatic gene expression induced by chromic exposure to high levels of the SV40 LT/st oncoproteins (4P)

ORGANISM(S): Mus musculus

PROVIDER: GSE5958 | GEO | 2014/12/22

SECONDARY ACCESSION(S): PRJNA97421

REPOSITORIES: GEO

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Alterations in hepatic gene expression induced by chronic exposure to low levels of the SV40 LT/st oncoproteins (4C)

Project description:Hepatic gene expression induced by chromic exposure to low levels of the SV40 LT/st oncoproteins (4P)

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Alterations in hepatic gene expression induced by chromic exposure to high levels of the SV40 LT/st oncoproteins (4P)

Project description:Hepatic gene expression induced by chromic exposure to high levels of the SV40 LT/st oncoproteins (4P) Affymetrix mouse genome U74Av2 platform was used, duplicate measurements for wild-type and transgenic animals

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Alterations in hepatic gene expression induced by chronic exposure to low levels of the SV40 LT/st oncoproteins (4C)

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Hepatic gene expression in transgenic mice with conditional liver-specific expression of the SV40 17kT/LT oncoproteins

Project description:The SV40 large (LT) and small (st) antigens are produced from a single alternatively spliced pre-mRNA, that when co-expressed, transform a variety of cells in vitro and in vivo. However, 17kT, a relatively uncharacterized third protein that is co-linear with LT for the first 131 amino acids, is also produced from the early viral pre-mRNA by removal of an additional intron from the LT transcript. Here we report a line of transgenic mice expressing a liver-specific dox-inducible viral transcript that fails to yield any detectable LT protein, yet produces abundant 17kT. Comparative analysis of livers of transgenic mice expressing either 17kT or LT demonstrates that while 17kT is a potent stimulator of cell proliferation, it is ineffective at inducing liver tumor development, due in part, to the failure of 17kT to effectively induce the expression of growth regulators and reactivate expression of imprinted and developmentally regulated hepatic genes. These studies highlight key functional differences between LT and 17kT in their ability to transform quiescent primary epithelial cells in vivo, and demonstrate how specific functional domains within LT impact cell-specific gene expression to promote oncogenesis. Keywords: genetic modification, SV40, 17kT, LT, Rb, p53, hepatocellular carcinoma, hepatic hyperplasia, differentiation.

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Hepatic gene expression in transgenic mice with conditional liver-specific expression of the SV40 17kT/LT oncoproteins

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Mammary carcinomas in WAP-SV40 transgenic mice [aCGH]

Project description:Transgenic expression in mice of two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens, in the mammary epithelium recapitulates loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated mammary adenocarcinomas. We performed a correlative aCGH and gene expression analysis of 25 monofocal tumors, representing four histopathological grades, to explore the molecular traits of SV40-induced mammary tumors and to emphasize the relevance of this tumor model for human breast tumorigenesis.

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Mammary carcinomas in WAP-SV40 transgenic mice [gene expression]

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Project description:Alterations in hepatic gene expression induced by chromic exposure to high levels of the SV40 LT/st oncoproteins (4P)

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Gene expression profiling of LT-HSCs and ST-HSCs conditionally expressing MLL-ENL

Project description:We have developed a new conditional transgenic mouse showing that MLL-ENL, at an endogenous-like expression level, induces leukemic transformation selectively in LT-HSCs. To investigate the molecular mechanism of leukemic transformation in LT-HSCs conditionally expressing MLL-ENL, we preliminarily performed comprehensive gene expression profiling of CreER-transduced LT-HSCs and ST-HSCs using cDNA microarray analysis.

2013-07-17 | GSE48539 | GEO

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