Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA388937 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The aim of this project is to determine the differential expression of genes between poorly differntiated HCC tumor compared to differntiated tumor arising in HCC/LECT2-KO mice
2018-08-13 | GSE99568 | GEO
Project description:The aim of this project is to determine the differential expression of genes between monocytes infiltrating HCC nodules in the absence versus in the presence of LECT2
2018-08-13 | GSE99569 | GEO
Project description:Common genetic traits are not well defined in hepatocellular carcinoma (HCC), because necroinflammation lasting long in prior to hepatocarcinogenesis embeds highly heterogenous genetic background in hepatocytes over the liver. We experienced a rare case with chronic hepatitis C, in which multiple liver tumors at different stages in multistep hepatocarcinogenesis were observed at the same time. Under the same genetic and etiological backgrounds, comparisons of expression profiles among dysplastic nodules (DN), well differentiated HCC (WEL), and moderately differentiated HCC (MOD) would provide critical genetic information for the initiation and progression of HCC.
2020-07-24 | GSE153565 | GEO
Project description:Mouse models of hepatocellular carcinoma (HCC) simulate specific subgroups of human HCC. We investigated hepatocarcinogenesis in Mdr2-KO mice, a model of inflammation-associated HCC, using gene expression profiling and immunohistochemical analyses. Gene expression profiling demonstrated that although Mdr2-KO mice differ from other published murine HCC models, they share several important deregulated pathways and many coordinately differentially expressed genes with human HCC datasets. Analysis of genome positions of differentially expressed genes in liver tumors revealed a prolonged region of down-regulated genes on murine chromosome 8 in three of the six analyzed tumor samples. This region is syntenic to human chromosomal regions that are frequently deleted in human HCC and harbor multiple tumor suppressor genes. Real-time RT-PCR analysis of 16 tumor samples confirmed down-regulation of several tumor suppressors in most tumors. We demonstrate that in the aged Mdr2-KO mice, cyclin D1 nuclear level is increased in dysplastic hepatocytes that do not form nodules; however, it is decreased in dysplastic nodules and in liver tumors. We found that this decrease is mostly at the protein, rather than the mRNA level. These findings raise the question on the role of cyclin D1 at early stages of hepatocarcinogenesis in the Mdr2-KO HCC model. Furthermore, we show that most liver tumors in Mdr2-KO mice were characterized by the absence of b-catenin activation. In conclusion, the Mdr2-KO mouse may serve as a model for b-catenin-negative subgroup of human HCCs characterized by low nuclear cyclin D1 levels in tumor cells and by down-regulation of multiple tumor suppressor genes. Experiment Overall Design: The liver RNA samples from six Mdr2-KO tumors, six non-tumorous liver tissues (four matched and two unmatched), as well as from three control heterozygous mice at 16 months of age were subjected to gene expression profiling using the genome scale Affymetrix Mouse Genome 430 2.0 Array.
2008-06-16 | E-GEOD-8642 | biostudies-arrayexpress
Project description:Aberrant expression of microRNA (miRNA) is closely associated with carcinogenesis. The malignancy of the hepatocellular carcinoma (HCC) is prescribed in the degree of histological differentiation. Poorly differentiated HCC is generally more malignant prognosis than well differentiated HCC. We analyzed the miRNA expression profiles in 110 HCC (60 moderately differentiated, 30 poorly differentiated, and 20 well differentiated HCC) by using microarray in order to establish the novel biomarker for the degree of histological differentiation and forecasting relapse of HCC. The expression level of 12 miRNAs was significantly different according to the degree of histological differentiation. The expression level of miR-18b in poorly differentiated HCC was significantly higher than that in well differentiated HCC. Based on the target search algorithm and argonaute 2 (Ago2) immunoprecipitation study for target binding assay, miR-18b can control the expression of trinucleotide repeat containing 6B (TNRC6B) as a target. Over expression of miR-18b and down regulation of TNRC6B accelerated the activity of cell proliferation and lost ability of cell adhesion in two hepatoma cell lines. Low expression of miR-18b is significantly decreased the relapse free rate after surgical resection. In conclusion, expression pattern of miR-18b is a marker of an important determinant in the control of cell proliferation and adhesion and also prediction of clinical course. From a clinical point of view, our study emphasizes miR-18b as a diagnostic and prognostic marker for HCC progression.
2013-04-10 | GSE31164 | GEO
Project description:Gene expression profile of poorly differentiated synovial sarcoma
| PRJNA125699 | ENA
Project description:Transcriptional profile comparing murine monocytes infiltrating HCC tumors in the absence/presence of LECT2 expression in the liver
| PRJNA388938 | ENA
Project description:Mouse models of hepatocellular carcinoma (HCC) simulate specific subgroups of human HCC. We investigated hepatocarcinogenesis in Mdr2-KO mice, a model of inflammation-associated HCC, using gene expression profiling and immunohistochemical analyses. Gene expression profiling demonstrated that although Mdr2-KO mice differ from other published murine HCC models, they share several important deregulated pathways and many coordinately differentially expressed genes with human HCC datasets. Analysis of genome positions of differentially expressed genes in liver tumors revealed a prolonged region of down-regulated genes on murine chromosome 8 in three of the six analyzed tumor samples. This region is syntenic to human chromosomal regions that are frequently deleted in human HCC and harbor multiple tumor suppressor genes. Real-time RT-PCR analysis of 16 tumor samples confirmed down-regulation of several tumor suppressors in most tumors. We demonstrate that in the aged Mdr2-KO mice, cyclin D1 nuclear level is increased in dysplastic hepatocytes that do not form nodules; however, it is decreased in dysplastic nodules and in liver tumors. We found that this decrease is mostly at the protein, rather than the mRNA level. These findings raise the question on the role of cyclin D1 at early stages of hepatocarcinogenesis in the Mdr2-KO HCC model. Furthermore, we show that most liver tumors in Mdr2-KO mice were characterized by the absence of b-catenin activation. In conclusion, the Mdr2-KO mouse may serve as a model for b-catenin-negative subgroup of human HCCs characterized by low nuclear cyclin D1 levels in tumor cells and by down-regulation of multiple tumor suppressor genes. Keywords: Hepatocellular carcinoma, Mouse model, Mdr2-knockout.
2007-10-10 | GSE8642 | GEO
Project description:Transcriptional profile of HCC nodules and their infiltrating monocytes
| PRJNA388872 | ENA
Project description:LECT2 is a liver derived cytokine and involved in many pathologic conditions, especially in immune regulation. To better understand cellular and molecular mechanisms of LECT2 in immune response, mouse peritoneal macrophages were isolated from mouse peritonaeum. After treatment with 0, 0.5 or 5 μg/ml of LECT2 for 3.5 or 48 hours, gene expression profile in mouse peritoneal macrophages was measured using gene expression array. Results showed that LECT2 treatment led to the enhancement of cytokines secretion and phagocytosis in peritoneal macrophages.
2011-12-13 | GSE33721 | GEO