Spelling suggestions: "subject:"river - aancer - animal models."" "subject:"river - aancer - 1animal models.""
1 |
AN EVALUATION OF THE NEWBORN MOUSE AS A POTENTIAL MODEL FOR THE BIOASSAY OF LIVER CARCINOGENESIS USING HISTOLOGICAL AND HISTOCHEMICAL MARKERS.Cater, Kathleen Carmelle. January 1982 (has links)
No description available.
|
2 |
The kringle 1 domain of hepatocyte growth factor exerts both anti-angiogenic and anti-tumor cell effects on hepatocellular carcinomaShen, Zan., 沈贊. January 2008 (has links)
published_or_final_version / Chemistry / Doctoral / Doctor of Philosophy
|
3 |
Identification of liver tumour-initiating cells using a chemoresistantanimal modelCastilho, Antonia Genevieve. January 2010 (has links)
published_or_final_version / Pathology / Master / Master of Philosophy
|
4 |
Significance of LRP6 coreceptor upregulation in the aberrant activation of Wnt signaling in hepatocellular carcinomaWong, Yin-chi, Betty., 黃妍之. January 2008 (has links)
published_or_final_version / Pathology / Master / Master of Philosophy
|
5 |
Role of microRNA-709 in murine liverSurendran, Sneha January 2014 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / MicroRNAs are small RNA molecules that regulate expression of genes involved in development, cell differentiation, proliferation and death. It has been estimated that in eukaryotes, approximately 0.5 to 1% of predicted genes encode a microRNA, which in humans, regulate at least 30% of genes at an average of 200 genes per miRNA. Some microRNAs are tissue-specific, while others are ubiquitously expressed. In liver, a few microRNAs have been identified that regulate specialized functions. The best known is miR-122, the most abundant liver-specific miRNA, which regulates cholesterol biosynthesis and other genes of fatty acid metabolism; it also regulates the cell cycle through inhibition of cyclin G1. To discover other miRNAs with relevant function in liver, we characterized miRNA profiles in normal tissue and identified miR-709. Our data indicates this is a highly abundant hepatic miRNA and is dysregulated in an animal model of type 2 diabetes. To understand its biological role, miR-709 gene targets were identified by analyzing the transcriptome of primary hepatocytes transfected with a miR-709 mimic. The genes identified fell within four main categories: cytoskeleton binding, extracellular matrix attachment, endosomal recycling and fatty acid metabolism. Thus, similar to miR-122, miR-709 downregulates genes from multiple pathways. This would be predicted, given the abundance of the miRNA and the fact that the estimated number of genes targeted by a miRNA is in the hundreds. In the case of miR-709, these suggested a coordinated response during cell proliferation, when cytoskeleton remodeling requires substantial changes in gene expression. Consistently, miR-709 was found significantly upregulated in an animal model of hepatocellular carcinoma. Likewise, in a mouse model of liver regeneration, mature miR-709 was increased. To study the consequences of depleting miR-709 in quiescent and proliferating cells, primary hepatocytes and hepatoma cells were cultured with antagomiRs (anti-miRs). The presence of anti-miR-709 caused cell death in proliferating cells. Quiescent primary hepatocytes responded by upregulating miR-709 and its host gene, Rfx1. These studies show that miR-709 targets genes relevant to cystokeleton structural genes. Thus, miR-709 and Rfx1 may be needed to facilitate cytoskeleton reorganization, a process that occurs after liver injury and repopulation, or during tumorigenesis.
|
Page generated in 0.065 seconds