Gene expression profile of c-MYC driven mouse liver tumours, compared with Normal livers from control mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA529706 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:Differentially expressed genes in Mettl3-deficient livers compared to control livers
| PRJNA812058 | ENA
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
Project description:Purpose: Human papilloma virus (HPV) associated head and neck squamous cell carcinoma (HNSCC) has a better prognosis than HPV(-) negative cancer. This may be due, in part, to the higher number of tumour infiltrating lymphocytes (TIL) in HPV(+) tumours. We used RNAseq to evaluate whether these differences in clinical behaviour could be explained simply by a numerical difference in TILs or whether there was a fundamental difference between TILs in these two settings. Patients and methods: Twenty-three consecutive HNSCC cases with high and moderate TIL density were subjected to RNAseq analysis. Differentially expressed genes (DEG) between 10 HPV(+) and 13 HPV(-) tumours were identified with EdgeR. Immune subset analysis was performed using, FAIME (Functional Analysis of Individual Microarray Expression) and Immune gene transcript count analysis. Results: 1634 genes were differentially expressed. There was a dominant immune signature in HPV(+) tumours. After normalizing expression profiles for numerical differences in T cells and B cells, 437 significantly DEGs still remained. A B-cell associated signature emerged, which segregated HPV(+) from HPV(-) cancers and included CD200, STAG3, GGA2, SPIB and ADAM28. Differential expression of these genes was confirmed by real-time quantitative PCR and immunohistochemistry. Conclusion: In our dataset, the difference associated with T-cells between patients with HPV(+) and (-) HNSCC was predominantly numerical. However, when TIL numbers are corrected, a distinct differential B-cell signature was revealed. mRNA profiles of 10 HPV driven (HPV+) and 13 HPV independant (HPV-) head and neck squamous cell carcinoma (HNSCC) tumours were generated by RNA-Seq, using Illumina HiSeq 2000.
2016-09-01 | E-GEOD-72536 | biostudies-arrayexpress
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
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
Project description:Profiling of mouse mammary tumours that have developed in a mouse model expressing mutant Pik3ca^H1047R at endogenous level under control of the MMTV promoter (Tikoo et al., PLoS one 2012). Copy number variations in tumours (compared to matching liver DNA) were detected using Agilent Sureprint microarrays.
2016-06-04 | GSE47635 | GEO
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.
2016-05-17 | GSE77729 | GEO
Project description:Blood exsosomal miRNAs of patients with normal livers, to be compared with liver diseas patients Aiming to develop circulatin biomarkers for liver disease, including progresson of fibrosis/inflammation. This data set should be uasd as control samples to be compared with liver disease patients.
2023-06-20 | GSE82301 | GEO
Project description:Genome-wide profiling for H2A.Z and genome accessibility using ATACseq in Uhrf1hepKO mouse livers compared to WT livers
| PRJNA641416 | ENA