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SnRNAseq of bCat-Kras tumors in normal and NASH diet

ABSTRACT: snRNAseq of bCat-Kras tumors in normal and NASH diet

PROVIDER: PRJNA1010346 | ENA |

REPOSITORIES: ENA

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snRNAseq of bCat-Kras tumors in normal and NASH diet

Project description:Current models of hepatocellular tumorigenesis propose that the chronic injury and inflammation in NASH are mutagenic and growth promoting which can eventually lead to HCC. However, contrary to this model, here we show that NASH suppresses the early development of liver cancers in mice. We found that NASH did not hinder the malignant reprogramming of oncogene expressing hepatocytes but suppressed their clonal expansion and led to their elimination. This elimination was not caused by a direct effect of NASH on malignant cells but due to the stimulation of cell competition in tumor-surrounding hepatocytes. Mechanistically, NASH activated the Hippo pathway effectors Yap and Taz in hepatocytes, which elevated their cellular fitness. Thus, deletion of Yap/Taz in tumor-surrounding hepatocytes abolished the elimination of tumor cells by NASH, while experimental hyperactivation of Yap in malignant cells protected them from NASH-induced elimination

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SnRNAseq of tumors isolated from Apc cKO; Kras-mutant animals

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NASH

Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays

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Project description:Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of disease that ranges from simple steatosis, to inflammatory form non-alcoholic steatohepatitis (NASH), cirrhosis, and up to hepatocellular carcinoma. While NASH usually takes decades to develop at a rate of one stage per seven years, in the case of post-trasplant NASH (pt-NASH) develops fibrosis much more rapidly, with almost 50% of liver transplant recipients presenting stage 3 fibrosis by 5 years post-transplant. Archived fresh-frozen transplanted liver biopsy samples from four liver biopsy samples with evidence of NASH (2 recurrent and 2 de novo), two with simple steatosis (both de novo), and five with normal histology as controls had their transcriptome sequenced in two batches for deeper coverage.

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snRNAseq of diffuse leptomeningeal glioneuronal tumors

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Murine lung tumors- HER2(V659E) and KRAS(G12V) vs normal lung

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Exosomal microRNA expression profiles of NASH: normal vs. NASH

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