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Gene expression profile of c-MYC driven mouse liver tumours, compared with Normal livers from control mice

ABSTRACT: Gene expression profile of c-MYC driven mouse liver tumours, compared with Normal livers from control mice

PROVIDER: PRJNA529706 | ENA |

REPOSITORIES: ENA

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Gene expression profile of c-MYC driven mouse liver tumours, compared with Normal livers from control mice

Project description:Liver tumours are induced by overexpresion of human c-MYC (LAP-tTA/tet-o-MYC) Using Affymetrix microarrays we compared gene expression of both tissues

2020-03-27 | GSE129013 | GEO

Modeling the MYC-driven normal-to-tumour switch in breast cancer.

Project description:The potent MYC oncoprotein is deregulated in many human cancers, including breast carcinoma, and is associated with aggressive disease. To understand the mechanisms and vulnerabilities of MYC-driven breast cancer, we have generated an in vivo model that mimics human disease in response to MYC deregulation. MCF10A cells ectopically expressing a common breast cancer mutation in the PI3 kinase pathway (PIK3CAH1047R) lead to the development of organized acinar structures in mice. However, expressing both PIK3CAH1047R and deregulated-MYC lead to the development of invasive ductal carcinoma, thus creating a model in which a MYC-dependent normal-to-tumour switch occurs in vivo. These MYC-driven tumours exhibit classic hallmarks of human breast cancer at both the pathological and molecular levels. Moreover, tumour growth is dependent upon sustained deregulated MYC expression, further demonstrating addiction to this potent oncogene and regulator of gene transcription. We therefore provide a MYC-dependent model of breast cancer which can be assayed for in vivo tumour initiation, proliferation, and transformation from normal breast acini into invasive breast carcinoma. Taken together, we anticipate that this novel MYC-driven transformation model will be a useful research tool to both better understand MYC’s oncogenic function and identify therapeutic vulnerabilities.

2019-07-25 | GSE130513 | GEO

Progression of KRas^G12D;Rosa26-MYC tumours to invasive disease

Project description:The aim of the study was to investigate gene expression tumour progression of KRas*/MYC driven lung tumours from adenocarcinoma in situ to invasive disease.

2018-06-01 | E-MTAB-6432 | biostudies-arrayexpress

MYC-driven mouse HCC proteomics

Project description:To identify proteomic signatures associated with hepatocellular carcinoma driven by MYC overexpression, proteomics was performed on the LAP-tTA/tetO-MYC mouse conditional liver cancer model. Upon MYC activation, mice form liver cancer. Differential proteomics was performed in "MYC on" (MYC-HCC) mouse liver tumors versus mouse control normal liver tissue (where MYC was not overexpressed to drive tumorigenesis -- "MYC off").

2022-10-12 | PXD031478 | Pride

Transcriptional profiling of intestinal changes in Apc Kras tumours with MYC activation and/or drug combination treatment

Project description:Transcriptional profiling of intestinal changes in Apc Kras tumours with MYC activation and/or drug combination treatment

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Progression of KRas^G12D Rosa26-MYC tumours to invasive disease

Project description:Progression of KRas^G12D Rosa26-MYC tumours to invasive disease

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RNAseq Expression data for mouse liver, Phenobarbital exposed livers and resulting liver tumours.

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. We carry out paired end , strand specific RNAseq prior to sequencing on Illumina Hiseq 2500 to report on the transcriptional landscape in replicate control mouse livers (n=2), 12 week Phenobarbital exposed livers (n=2)and resulting (35 week PB) liver tumours (n=3).

2016-05-17 | E-GEOD-77729 | biostudies-arrayexpress

mRNA expression data from livers of wild-type (WT) mice, mice that lack ribosomal protein S6 (Rps6) (DS6), mice that overexpress c-Myc (Myc) and livers that lack Rps6 and also overexpress c-Myc (DS6 Myc)

Project description:Targeted depletion of ribosomal protein S6 (Rps6) from hepatoblasts of the developing liver results in neonatal sub-lethal hepatic failure due to inhibition of bile duct development and widespread induction of hepatocyte death triggering regeneration. Overexpression of c-Myc is hepatoprotective in the context of Rps6-deficiency and eliminates the need for DS6 livers to regenerate by preventing hepatocyte death. Microarrays were used to identify the transcriptional program associated with loss of hepatic Rps6 and to identify mRNAs associated with c-Myc's hepatoprotective effect in DS6 livers

2023-01-04 | GSE212363 | GEO

Gene expression profile of overgrown livers from genetic models involving YAP or MYC overexpression.

Project description:We reasoned that when livers grow beyond their normal size, some growth regulating secreted factors will be suppressed and others will be overexpressed. To obtain overgrown livers, we used genetic models involving YAP or MYC overexpression We the identified differentially expressed genes in both models and filtered out secreted factors by bioinformatically defined secreted protein list.

2024-04-01 | GSE228863 | GEO

Expression of genes in Runx2/Myc transgenic mouse thymus compared to control

Project description:Retroviral insertional mutagenesis (RIM) is a powerful tool in cancer genomics. Transgenic mice expressing two potent collaborating oncogenes in the germline, Myc and Runx2, develop rapid onset tumours that can be accelerated and rendered polyclonal by neonatal infection with MoMLV. Deep sequencing of lymphomas from infected Runx2/Myc mice revealed a network of progression genes. Transcriptional analysis of basal expression levels in transgenic cells showed that the progression network showed strong evidence of clonal selection beyond gene expression level. We examined the gene expression profile of triplicate 10 day old thymus from CD2-Myc/CD2-Runx2 and C57/CBA mice to examine early gene changes in comparison to RIM targets in end stage tumours. We found no significant relationship between basal expression in the transgenic system and genes that were targets for retroviral integration.

2016-04-14 | E-GEOD-80254 | biostudies-arrayexpress

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