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ABSTRACT:
PROVIDER: PRJNA132793 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the following subset Series: GSE29846: Genomic profiles of mouse liver tissue harboring deletion of RB and/or p53, untreated or post-hepatocarcinogen treatment [expression data] GSE29847: Genomic profiles of mouse liver tissue harboring deletion of RB and/or p53, untreated or post-hepatocarcinogen treatment [CGH data] Refer to individual Series
2011-09-19 | E-GEOD-24347 | biostudies-arrayexpress
Project description:Genomic profiles of mouse liver tissue harboring deletion of RB and/or p53, untreated or post-hepatocarcinogen treatment [expression data]
| PRJNA141009 | ENA
Project description:Genomic profiles of mouse liver tissue harboring deletion of RB and/or p53, untreated or post-hepatocarcinogen treatment [CGH data]
| PRJNA141011 | ENA
Project description:The retinoblastoma (RB) and p53 tumor suppressors are critical regulators of the cell cycle with profound impact on both normal cell biology and disease etiology. In the context of human cancers, compound inactivation of RB and p53 is a frequent occurrence; however, the cooperation of these tumor suppressors in driving tumorigenesis has proven to be intricate and dependent on both the tissue and type of cancer. Hepatocellular carcinoma (HCC) is a highly complex disease characterized by numerous molecular abnormalities (e.g. p53, RB, TGFβ) and chromosomal aberrations associated with environmental factors (e.g. Hepatitis B/C Virus, Aflatoxin B1). Despite extensive research, how each of these facets of disease development cooperates in promoting tumorigenesis is ultimately unknown. In the current study, we present a mouse model of liver tumorigenesis, in which the impact of RB and p53 loss is modified by the tissue environment. While loss of RB and p53 promotes deregulation of transcriptional programs associated with advanced disease, these changes are not sufficient to drive spontaneous tumorigenesis in the liver. However, in response to carcinogen-induced damage, distinct and cooperative roles of RB and p53 are revealed, which critically impact cell cycle control, checkpoint response, genome stability, and ultimately tumor development. Mice that are transgenic for Cre recombinase under the albumin promoter and harboring loxP sites within the Rb and/or p53 genes. For gene expression microarray analysis, mice were aged to 14 days, and treated for 24 hours with diethylnitrosamine (DEN) or saline as a control. For CGH analysis, mice were aged to 6 months post-DEN treatment. Liver tissue was obtained from dissected tumors and compared to normal liver tissue of 6-month old, saline-treated littermates. CGH analysis includes 5 individual tumor samples and 2 control samples (each consisting of a pool of 3 normal mouse liver DNA).
2011-09-19 | E-GEOD-29847 | biostudies-arrayexpress
Project description:The retinoblastoma (RB) and p53 tumor suppressors are critical regulators of the cell cycle with profound impact on both normal cell biology and disease etiology. In the context of human cancers, compound inactivation of RB and p53 is a frequent occurrence; however, the cooperation of these tumor suppressors in driving tumorigenesis has proven to be intricate and dependent on both the tissue and type of cancer. Hepatocellular carcinoma (HCC) is a highly complex disease characterized by numerous molecular abnormalities (e.g. p53, RB, TGFβ) and chromosomal aberrations associated with environmental factors (e.g. Hepatitis B/C Virus, Aflatoxin B1). Despite extensive research, how each of these facets of disease development cooperates in promoting tumorigenesis is ultimately unknown. In the current study, we present a mouse model of liver tumorigenesis, in which the impact of RB and p53 loss is modified by the tissue environment. While loss of RB and p53 promotes deregulation of transcriptional programs associated with advanced disease, these changes are not sufficient to drive spontaneous tumorigenesis in the liver. However, in response to carcinogen-induced damage, distinct and cooperative roles of RB and p53 are revealed, which critically impact cell cycle control, checkpoint response, genome stability, and ultimately tumor development. Mice that are transgenic for Cre recombinase under the albumin promoter and harboring loxP sites within the Rb and/or p53 genes. For gene expression microarray analysis, mice were aged to 14 days, and treated for 24 hours with diethylnitrosamine (DEN) or saline as a control. For CGH analysis, mice were aged to 6 months post-DEN treatment. Liver tissue was obtained from dissected tumors and compared to normal liver tissue of 6-month old, saline-treated littermates. CGH analysis includes 5 individual tumor samples and 2 control samples (each consisting of a pool of 3 normal mouse liver DNA).
2011-09-19 | E-GEOD-29846 | biostudies-arrayexpress
Project description:The RB and p53 tumor suppressor pathways regulate the transcription of genes involved in cell cycle progression, DNA replication, DNA repair, and apoptosis. These tumor suppressors are critical modulators of the response to genotoxic damage and both pathways are frequently inactivated in human cancers. We used microarrays to monitor gene expression patterns upon exposure to cisplatin treatment in fibroblasts harboring loss/inactivation of RB and/or p53. We generated mouse adult fibroblasts harboring loss/inactivation of RB and/or p53 and subjected these cell populations to cisplatin treatment for 24 hours. Treated cell populations were allowed to recover from cisplatin exposure, generating a recurred cell popuation. Untreated and recurred cell populations were then subjected to RNA extraction and hybridization on Affymetrix microarrays.
2010-10-01 | E-GEOD-18395 | biostudies-arrayexpress
Project description:Addition of liver-specific Keap1 deletion to mice harboring mutant K-ras and p53 accelerated cholangiocarcinoma formation, with hallmarks of Nrf2 activation.
2021-09-27 | GSE138101 | GEO
Project description:The retinoblastoma (RB) and p53 tumor suppressors are critical regulators of the cell cycle with profound impact on both normal cell biology and disease etiology. In the context of human cancers, compound inactivation of RB and p53 is a frequent occurrence; however, the cooperation of these tumor suppressors in driving tumorigenesis has proven to be intricate and dependent on both the tissue and type of cancer. Hepatocellular carcinoma (HCC) is a highly complex disease characterized by numerous molecular abnormalities (e.g. p53, RB, TGFβ) and chromosomal aberrations associated with environmental factors (e.g. Hepatitis B/C Virus, Aflatoxin B1). Despite extensive research, how each of these facets of disease development cooperates in promoting tumorigenesis is ultimately unknown. In the current study, we present a mouse model of liver tumorigenesis, in which the impact of RB and p53 loss is modified by the tissue environment. While loss of RB and p53 promotes deregulation of transcriptional programs associated with advanced disease, these changes are not sufficient to drive spontaneous tumorigenesis in the liver. However, in response to carcinogen-induced damage, distinct and cooperative roles of RB and p53 are revealed, which critically impact cell cycle control, checkpoint response, genome stability, and ultimately tumor development.
2011-09-20 | GSE29847 | GEO
Project description:The retinoblastoma (RB) and p53 tumor suppressors are critical regulators of the cell cycle with profound impact on both normal cell biology and disease etiology. In the context of human cancers, compound inactivation of RB and p53 is a frequent occurrence; however, the cooperation of these tumor suppressors in driving tumorigenesis has proven to be intricate and dependent on both the tissue and type of cancer. Hepatocellular carcinoma (HCC) is a highly complex disease characterized by numerous molecular abnormalities (e.g. p53, RB, TGFβ) and chromosomal aberrations associated with environmental factors (e.g. Hepatitis B/C Virus, Aflatoxin B1). Despite extensive research, how each of these facets of disease development cooperates in promoting tumorigenesis is ultimately unknown. In the current study, we present a mouse model of liver tumorigenesis, in which the impact of RB and p53 loss is modified by the tissue environment. While loss of RB and p53 promotes deregulation of transcriptional programs associated with advanced disease, these changes are not sufficient to drive spontaneous tumorigenesis in the liver. However, in response to carcinogen-induced damage, distinct and cooperative roles of RB and p53 are revealed, which critically impact cell cycle control, checkpoint response, genome stability, and ultimately tumor development.
2011-09-20 | GSE29846 | GEO
Project description:Our findings suggested that cytokines were upregulated in p53 null primary prostate cells after deleting Rb. Rb deletion is important for prostate cancer progression. p53-/- Rbf/f vs p53-/- Rbâf/âf primary prostate cells.Three independent experiments were performed.
2015-12-31 | E-GEOD-68903 | biostudies-arrayexpress