Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA393221 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In vivo reprogramming drives Kras-induced cancer development [expression]
| PRJNA393220 | ENA
Project description:In vivo reprogramming drives Kras-induced cancer development
| PRJNA393216 | ENA
Project description:Accumulation of genetic mutations is thought to be a primary cause of cancer. However, a set of genetic mutations sufficient for cancer development remains unclear in most cancers, including pancreatic cancer. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We first demonstrate that Kras and p53 mutations are insufficient to induce activation of ERK signaling and cancer development in the pancreas. We next show that short transient expression of reprogramming factors (1-3 days) in pancreatic acinar cells results in repression of acinar cell enhancers and reversible loss of acinar cell properties. Notably, the transient expression of reprogramming factors in Kras mutant mice is sufficient to induce robust and persistent activation of ERK signaling in acinar cells and rapid formation of pancreatic ductal adenocarcinoma (PDAC). In contrast, forced expression of acinar cell-related transcription factors inhibits pancreatitis-induced activation of ERK signaling and development of precancerous lesions in Kras-mutated acinar cells.
2018-05-16 | GSE100840 | GEO
Project description:Accumulation of genetic mutations is thought to be a primary cause of cancer. However, a set of genetic mutations sufficient for cancer development remains unclear in most cancers, including pancreatic cancer. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We first demonstrate that Kras and p53 mutations are insufficient to induce activation of ERK signaling and cancer development in the pancreas. We next show that short transient expression of reprogramming factors (1-3 days) in pancreatic acinar cells results in repression of acinar cell enhancers and reversible loss of acinar cell properties. Notably, the transient expression of reprogramming factors in Kras mutant mice is sufficient to induce robust and persistent activation of ERK signaling in acinar cells and rapid formation of pancreatic ductal adenocarcinoma (PDAC). In contrast, forced expression of acinar cell-related transcription factors inhibits pancreatitis-induced activation of ERK signaling and development of precancerous lesions in Kras-mutated acinar cells.
2018-05-16 | GSE100841 | GEO
Project description:We examine the potential of Kras as a metabolic target in lung cancer using the KrasLSL-G12D lung cancer model. We demonstrate that mutant Kras drives a lipogenic gene expression program, and that fatty acid synthesis is important in Kras-induced tumorigenesis. Compare gene expression changes between mutant Kras (G12D) driven lung tumors and normal lung samples to identify pathways selectively altered in lung tumors.
2018-04-27 | GSE113717 | GEO
Project description:Electromagnetic field-mediated direct lineage reprogramming into induced dopamine neurons in vivo for Parkinson’s disease therapy [ChIP-Seq]
| PRJNA340137 | ENA
Project description:Phase separation drives aberrant chromatin looping and cancer development [ChIP-Seq]
| PRJNA602701 | ENA
Project description:Pericyte induced reprogramming of the bone marrow microenvironment drives stem and cancer cell quiescence
2018-09-17 | E-MTAB-6872 | ExpressionAtlas
Project description:In vivo reprogramming provokes a wide range of cell fate conversion. Here, we discover that in vivo induction of higher levels of OSKM in mouse somatic cells leads to increased expression of primordial germ cell (PGC)-related genes and provokes genome-wide erasure of genomic imprinting, which takes place exclusively in PGCs. Moreover, the in vivo OSKM reprogramming results in development of cancer that resembles human germ cell tumors. Like a subgroup of germ cell tumors, propagated tumor cells differentiate into trophoblasts. Moreover, these tumor cells give rise to induced pluripotent stem cells (iPSCs) with expanded differentiation potential into trophoblasts. Remarkably, the tumor-derived iPSCs are able to contribute to non-neoplastic somatic cells in adult mice. Mechanistically, DMRT1, which is expressed in PGCs, drives the reprogramming and propagation of the tumor cells in vivo. Furthermore, the DMRT1-related epigenetic landscape is associated with trophoblast competence of the reprogrammed cells and provides a therapeutic target for germ cell tumors. These results reveal an unappreciated route for somatic cell reprogramming and underscore the impact of reprogramming in development of germ cell tumors.
2021-07-20 | GSE149499 | GEO
Project description:TCDD is an environmental contaminant that elicits a number of hepatic effects including fat accumulation, inflammation, and fibrosis that can progress to hepatocellular carcinoma. RNA-Seq and targeted metabolomics were integrated with complementary dioxin response element (DRE) location and aryl hydrocarbon receptor (AhR) ChIP-Seq data to further investigate the hepatotoxicity of TCDD. Our integrative analysis identified changes similar to the Warburg effect observed in cancer cells, including pyruvate kinase isoform switching (PKM1 to PKM2), and an increase in the glutaminase (GLS1) GAC:KGA isoform ratio. Consequently, metabolites are redirected towards the pentose phosphate pathway, serine biosynthesis, and glutaminolysis. We propose that the effects of TCDD on central carbon and amino acid metabolism represents AhR-mediated hepatic metabolic reprogramming in order to increase NADPH production as an oxidative stress counter-measure.
2017-02-02 | MTBLS225 | MetaboLights