Gene expression in murine T-ALL following titrated MYC inactivation
Ontology highlight
ABSTRACT: 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.
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.
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)
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
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").
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.
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.
Project description:P493-6 cells are immortalized human peripheral B cells that carry a conditional, tetracycline-regulated myc gene. We present ChIP-seq analysis of key transcritional regulators in P493-6 cells expressing various levels of c-Myc: 0hr (low c-Myc levels), 1hr (intermediate c-Myc levels), 24hr (very high c-Myc levels) and No Tet (steady-state c-Myc levels). Brd4, c-Myc, Max, Med1, RNAPII, and the chromatin modification H3K27Ac were profiled in P493-6 cells
Project description:P493-6 cells are immortalized human peripheral B cells that carry a conditional, tetracycline-regulated myc gene. We present ChIP-seq analysis of key transcritional regulators in P493-6 cells expressing various levels of c-Myc: 0hr (low c-Myc levels), 1hr (intermediate c-Myc levels), 24hr (very high c-Myc levels) and No Tet (steady-state c-Myc levels).
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.
Project description:We previously described the use of a spotted oligonucleotide array to identify the mir-17 cluster as a direct transcriptional target of Myc. In order to determine whether Myc regulates additional miRNAs, we produced custom microarrays with an expanded set of probes capable of assaying the expression of 313 human miRNAs and 233 mouse miRNAs. P493-6 cells which are Epstein-Barr virus-immortalized human B cells that harbor a tetracycline (tet)-repressible allele of Myc were studied. These cells are tumorigenic in immunocompromised mice and represent a model of human B cell lymphoma. miRNA expression profiles were examined in the high Myc (-tet) and low Myc (+tet) state. Keywords: Dose response P493 cells with high Myc (-tet) and low Myc (+tet) were compared.