Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transgenic Eµ-myc mouse lymphoma array CGH data

ABSTRACT: We used array CGH data from Eµ-myc lymphomas to assess significant differences in DNA copy number variation between Cluster 1 and Cluster 2 lymphomas. When Eµ-myc mice had evidence of lymphoma and/or ill appearance, they were humanely sacrificed and dissected. Lymphoma tissue was obtained and flash frozen in liquid nitrogen. Later, lymphoma tissue was homogenized, and genomic DNA was extracted. Array CGH was performed on genomic DNA, with genomic DNA from normal background strain mice used as the reference.

ORGANISM(S): Mus musculus

SUBMITTER: Daphne Friedman

PROVIDER: E-GEOD-40759 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

The Eµ-myc Mouse Model Represents Heterogeneity Across Human Aggressive B-cell Lymphomas

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-09-10 | E-GEOD-40760 | biostudies-arrayexpress

Transgenic Eµ-myc mouse lymphoma expression data for test dataset [Mouse430_2]

Project description:We used gene expression data from Eµ-myc mouse lymphomas to test various genomic signatures and select lymphomas for further study When Eµ-myc mice had evidence of lymphoma and/or ill appearance, they were humanely sacrificed and dissected. Lymphoma tissue was obtained and flash frozen in liquid nitrogen. Lymphoma was dissociated into a single cell suspension, and cell pellets were frozen. Later, lymphoma tissue or cells were homogenized, and RNA was extracted. Gene expression microarrays were performed with the isolated RNA.

2014-09-10 | E-GEOD-40757 | biostudies-arrayexpress

Transgenic Eµ-myc mouse lymphoma expression data for training dataset

Project description:We used gene expression data from Eµ-myc mouse lymphomas to perform unsupervised analyses that identified two lymphoma subgroups. We also used this data to develop a genomic signature to classify new lymphomas. When Eµ-myc mice had evidence of lymphoma and/or ill appearance, they were humanely sacrificed and dissected. Lymphoma tissue was obtained and flash frozen in liquid nitrogen. Later, lymphoma tissue was homogenized, and RNA was extracted. Gene expression microarrays were performed with the isolated RNA.

2014-09-10 | E-GEOD-40756 | biostudies-arrayexpress

Transgenic Eµ-myc mouse lymphoma expression data for test dataset [Mouse430A_2]

Project description:We used gene expression data from Eµ-myc mouse lymphomas to test various genomic signatures and select lymphomas for further study When Eµ-myc mice had evidence of lymphoma and/or ill appearance, they were humanely sacrificed and dissected. Lymphoma tissue was obtained and flash frozen in liquid nitrogen. Lymphoma and spleens were dissociated into single cell suspensions, and cell pellets were frozen. Later, lymphoma tissue or cells were homogenized, and RNA was extracted. Gene expression microarrays were performed with the isolated RNA.

2014-09-10 | E-GEOD-40758 | biostudies-arrayexpress

The effect on gene expression of Smchd1 deletion in end stage lymphomas

Project description:Smchd1 appears to act as a tumour suppressor in the Eµ-Myc B cell lymphoma model. We find gene expression differences are most pronounced in the premalignant cells, and observe more variability in end stage lymphomas. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis. The microarrays compared Smchd1 null and Smchd1 wildtype samples from end stage lymphomas. All lymphomas are on the C57BL/6 background and carry the Eµ-Myc transgene, and Smchd1 null samples are additionally homozygous for a Smchd1 genetrap allele.

2012-09-30 | E-GEOD-40880 | biostudies-arrayexpress

B cell Lymphomas present Immunoglobulin Neoantigens

Project description:Immunoglobulin gene rearrangement and somatic hypermutation have the potential to create neoantigens in non-Hodgkin B cell lymphoma. However, the presentation of these putative immunoglobulin neoantigens by B cell lymphomas has not been proven. We used MHC immunoprecipitation followed by liquid chromatography and tandem mass spectrometry (LC-MS/MS) to define antigens presented by follicular lymphomas (FL), chronic lymphocytic leukemias (CLL), diffuse large B cell lymphoma (DLBCL) and mantle cell lymphomas (MCL). We found presentation of the clonal immunoglobulin molecule, including neoantigens by both class I and class II MHC, though more commonly in class II MHC. To determine whether B cell activation could promote presentation of immunoglobulin neoantigens, we used a toll-like receptor 9 (TLR9) agonists to upregulate expression of MHC-II. This resulted in enhanced class II MHC presentation of the immunoglobulin variable region including neoantigens. These findings demonstrate that immunoglobulin neoantigens are presented across most subtypes of B cell lymphomas. Activation of lymphoma cells to upregulate antigen presentation boosts presentation of immunoglobulin neoantigens and represents a strategy for augmenting lymphoma immunotherapies.

2019-01-07 | PXD010808 | Pride

Expression profiling of Eµ-Myc-driven lymphomas using a reversible switchable p53 allele modeling early and late stage p53 inactivation.

Project description:For the most frequently inactivated tumor suppressor p53, genetic mouse models have demonstrated regression of p53-null tumors upon p53 reactivation. While this was shown in tumor models driven by p53 loss as the initiating lesion, many tumors initially develop in the presence of wild-type p53, acquire aberrations in the p53 pathway to bypass p53-mediated tumor suppression, and inactivate p53 itself only at later stages during metastatic progression or therapy. To explore the efficacy of p53 reactivation in this scenario, we used a reversibly switchable p53 (p53ERTAM) mouse allele to generate Eµ-Myc-driven lymphomas in the presence of active p53 and, after full lymphoma establishment, switched off p53 to model late-stage p53 inactivation.

2019-10-18 | E-MTAB-8015 | biostudies-arrayexpress

Transgenic Eµ-myc mouse lymphoma expression data for training dataset

2014-09-10 | GSE40756 | GEO

A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma [MALT dataset]

Project description:Attempts at modeling chromosomal translocations involving MALT1 gene, hallmarks of human mucosa-associated lymphoid tissue (MALT) lymphoma, have failed to reproduce the disease in mice. Here we describe a transgenic model in which MALT1 expression was targeted to mouse hematopoietic stem/progenitor cells. In Sca1-MALT1 mice, MALT1 deregulation activated the NF-kappaB pathway in Sca1+ cells, promoting selective B-cell differentiation and mature lymphocyte accumulation in extranodal tissues, progressively leading to the development of clonal B-cell lymphomas. These tumors recapitulated the histopathological features of human MALT lymphomas, presenting typical lymphoepithelial lesions and plasmacytic differentiation. Transcriptional profiling of Sca1-MALT1 murine lymphomas revealed overlapping molecular signatures with human MALT lymphomas, including MALT1-mediated NF-kappaB activation, pro-inflammatory signaling and XBP1-induced plasmacytic differentiation. Moreover, murine Malt1 showed proteolytic activity by cleaving Bcl10 in Sca1-MALT1 lymphomas. Our novel technological approach has allowed modeling human MALT lymphoma in mice, which represent unique tools study MALT lymphoma biology and evaluate anti-MALT1 therapies. Keywords: lymphoma profiling, MALT lymphoma 97 samples were analized of which 13 were normal B-cell purified subpopulations and 84 lymphoma samples (31 MALT lymphomas, 26 DLBCL, 15 FCL and 12 SMZL)

2012-07-09 | E-GEOD-25638 | biostudies-arrayexpress

A novel CRISPR activation mouse enables modelling of aggressive lymphoma and interrogation of venetoclax resistance

Project description:CRISPR technologies have advanced cancer modelling in mice, but CRISPR activation (CRISPRa) methods have not been exploited in this context. We establish a CRISPRa mouse (dCas9a-SAMKI/+ 38 ) for inducing gene expression in vivo and in vitro. Using dCas9a-SAMKI 39 primary lymphocytes, we induced B cell restricted genes in T cells and vice versa, demonstrating the power of this system. There are limited models of aggressive double hit lymphoma. Therefore, we transactivated pro-survival BCL-2 in Eµ-MycT/+;dCas9a-SAMKI/+ 42 haematopoietic stem and progenitor cells. Mice transplanted with these cells rapidly developed lymphomas expressing high BCL-2 and MYC. Unlike standard Eµ-Myc lymphomas, BCL-2 expressing lymphomas were highly sensitive to the BCL-2 inhibitor venetoclax. We performed genome-wide activation screens in these lymphoma cells and found a dominant role for the BCL-2 protein A1 in venetoclax resistance. Here we show the power of our CRISPRa model for mimicking disease and providing insights into resistance mechanisms towards targeted therapies.

2022-07-08 | GSE205509 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data