Project description:The scope of this project is to study, using state-of-the-art systems in the liver following den induced liver cancer with dietary modification (high fat diet and sugar water - HFD+SW).
Project description:The aim of this study was to evaluate the ability of a diet enriched with biologically active compounds to protect against 1,2-dimethylhydrazine - induced carcinogenesis in 14-month old rats liver.
Project description:The aim of this study was to evaluate the ability of a diet enriched with biologically active compounds to protect against 1,2-dimethylhydrazine - induced carcinogenesis in 14-month old rats liver. Rats from control and experimental groups after 14 months of experiment were given 5 times 1,2-dimethylhydrazine (DMH) by intraperitoneal treatment at a dose of 30mg/kg of body weight once a week to induce the process of carcinogenesis. RNA from their livers were hybridized to Agilent two color microarrays with a common reference. Then, the transcriptomic profile of these livers were compared to the transcriptomic profile of 14-month rats received the same control diet and diet enriched with biologically active substances, but without 1,2-dimethylhydrazine - induction (data from GEO Submission - GSE51657).
Project description:High fat diet and entotoxemia induced inlammation associated carcinogenesis at the esophagogastric junction tumor through inflammation associated The promotion of the carcinogenesis may be related to gut dysbiosis related to high fat diet.
Project description:The purpose of this experiment was to determine the murine liver expression traits that were changed in response to diet induced obesity. Keywords: diet induced obesity signature
Project description:We reported the hepatic gene expression profiling in mice treated by perfluorooctanoate (PFOA) and high fat diet (HFD). Chronic HFD treatment was associated with gene expression changes in cholesterol biosynthetic process, lipid metabolic process, extracellular matrix, and inflammatory response pathways. Many chemokine related genes including Ccl2, Ccr2, Ccl3l3, Cx3cl1, Cx3cr1, Cxcl14, and toll-like receptor (TLR) related genes including Tlr2, Tlr7, Tlr8, Tlr13 were all significant upregulated comparing vehicle-treated HFD-fed mice to control diet (CD)-fed mice, suggesting their roles in the development of steatohepatitis. PFOA induced gene expression changes in PPAR signaling, fatty acid degradation, biosynthesis of unsaturated fatty acids, and chemical carcinogenesis pathways regardless of diet. However, we showed preexisting fatty liver enhanced the lipid clearance effect of PFOA compared to that in a normal liver. At last, chronic exposure to HFD and PFOA was found to interact on genes related to PPAR signaling, chemical carcinogenesis, and ABC transporter pathways.
Project description:Comprehensive quantitative profile of diet-induced alterations of mouse liver mitochondrial proteome, protein acetylation and succinylation.
Project description:KrasG12D mutation and Mdm2 loss in the liver (LiKM) accelerated liver carcinogenesis in mice, compared with LiK (KrasG12D mutation in the liver) mice. Acyclic retinoid (ACR) diet suppressed tumor development in LiKM mice. The goal of RNA-seq of non-tumorous liver tissues is to identifiy the effect of ACR diet on the transcriptomic profile of the liver and clarify the mechamism of ACR-mediated tumor suppression in LiKM mice.
Project description:Examination of gene expression profiles from liver of C57BL/6 mice and LDL receptor deficient mice fed on either a low fat diet or a high fat Western-style diet for 12 weeks. Three replicates of each condition analyzed. Keywords = LDL receptor deficiency, high fat diet, atherosclerosis, liver Keywords: repeat sample
Project description:Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis.