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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE129013 | GEO | 2020/03/27

REPOSITORIES: GEO

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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

Gene Expression Analysis of Transgenic Myc-Driven Liver Tumor Formation and Regression

Project description:Gene expression changes were examined in transgenic MYC-driven liver cancers at different time points as tumors formed and upon early regression. Time points evaluated include: Control (non-tumor bearing), Pre-tumor (mice were removed from doxyclycine in their diet to induce MYC oncogene expression for 4-5 weeks), Tumor (tumor nodules from mice that had been off of doxycycline for 8-9 weeks) and Early tumor regression (tumor-bearing mice were placed back on doxycycline for 72 hrs to inhibit MYC oncogene expresion). MYC-Driven Mouse Tumor Models are described in Schahaf, et al., Nature, 2004 and Goga, et al., Nature Medicine, 2007. 11 Total Samples: 3 Control, 4 Pre-Tumor, 4 Tumor, 4 Early Tumor Regression. Control = LAP-tTA transgenic mice. Others = TRE-MYC x LAP-tTA double transgenic mice (doxy off).

2011-07-06 | E-GEOD-28198 | biostudies-arrayexpress

Gene Expression Differences in MYC and RAS Driven Liver Cancer Transgenic

Project description:MYC and RAS signaling are two oncogene pathways important in human liver cancer. We sought to model liver cancer driven by either MYC or RAS using conditional LAP-tTA crossed to either TRE-MYC or TRE-HRAS models in the FVB/N background, and to understand oncogenic signaling pathways that are distinct between each model. Non-tumor tissue, from LAP-tTTA (LT2) mice were used as controls. In this study, we generated tumors from either MYC or RAS driven tumors and compared global gene expression changes to each other and control samples.

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Project description:We analyzed the molecular changes in a mouse c-MET over-expression model of hepatocellular carcinoma (HCC). FVB mice overexpressing human c-MET carried one copy of the LAP-tTa transgene (the liver-specific LAP promoter driving the Tet-VP16 transactivator) and one copy of the TRE-c-MET transgene (Tet-operator regulated human c-MET gene). Normal liver or liver tumor tissue (two per mouse) was collected and processed for gene expression profiling.

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Gene expression in murine T-ALL following titrated MYC inactivation

Project description:To understand changes to gene expression in murine T-ALL following MYC inactivation, T-ALL cells were isolated from EμSRα-tTA/tet-O-MYC/FVB/N mice and treated with varying concentrations of doxycyline for 48 hours to place cells in the MYC on, MYC intermediate, or MYC off state.

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

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

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Time course of gene expression in murine T-ALL following MYC inactivation

Project description:To understand changes to gene expression over time in murine T-ALL following MYC inactivation, T-ALL cells were isolated from EμSRα-tTA/tet-O-MYC/FVB/N mice and treated with doxycyline to turn MYC off for varying amounts of time before assessing gene expression.

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MYC functions as a switch for natural killer cell-mediated immune surveillance of lymphoid malignancies

Project description:We delineate the immunobiology during MYC oncogene-driven lymphomagenesis by RNA sequencing analysis followed by CIBERSORT of bulk splenic samples from healthy and SRa-tTA/tet-O-MYC mice before and after MYC inactivation. The data set also delineates global changes in signaling molecules in healthy spleens (controls) and lymphomagenic spleens in MYC ON and MYC OFF states.

2020-04-20 | GSE106078 | GEO

Transgenic MYC OFF timecourse in murine MYC-dependent cell line

Project description:In this experiment we determine MYC-dependent changes in a MYC OFF time-course. Using the established 4188 cell line derived from the Eμ-tTA/Tet-O-MYC primary model of T-ALL, we performed RNA-seq at 0 (MYC ON), and 4, 8, 12, 24, and 48 hours after addition of 20ng/µl doxycycline (MYC OFF)

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Gene expression analysis of TIL rich HPV driven head and neck tumours reveals a distinct B-cell signature when compared to HPV independent tumours.

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.

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