Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

7 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PRDM11: a novel tumor suppressor

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

ORGANISM(S): Mus musculus

SUBMITTER: Anders Lund

PROVIDER: E-GEOD-56065 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Loss of PRDM11 promotes MYC-driven lymphomagenesis.

Fog Cathrine Kolster CK Asmar Fazila F Côme Christophe C Jensen Klaus Thorleif KT Johansen Jens Vilstrup JV Kheir Tony Bou TB Jacobsen Linda L Friis Carsten C Louw Alison A Rosgaard Louise L Øbro Nina Friesgaard NF Marquart Hanne Vibeke HV Anthonsen Kristian K Braat Arie Koen AK van Lohuizen Maarten M Ralfkiaer Elisabeth E Grønbæk Kirsten K Lund Anders Henrik AH

Blood 20141212 8

The PR-domain (PRDM) family of genes encodes transcriptional regulators, several of which are deregulated in cancer. By using a functional screening approach, we sought to identify novel tumor suppressors among the PRDMs. Here we demonstrate oncogenic collaboration between depletion of the previously uncharacterized PR-domain family member Prdm11 and overexpression of MYC. Overexpression of PRDM11 inhibits proliferation and induces apoptosis. Prdm11 knockout mice are viable, and loss of Prdm11 a ...[more]

PMID: 25499759

Similar Datasets

Expression data from EμMyc;Prdm11 WT and EμMyc;Prdm11 KO end-stage splenic tumors

Project description:The PR-domain family (PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We found that loss of Prdm11 accelerates MYC-driven lymphomagenesis in the Eµ-Myc mouse model. Expression data from EμMyc;Prdm11 WT and EμMyc;Prdm11 KO end-stage splenic tumors to identify genes deregulated by loss of Prdm11 9 EμMyc;Prdm11 WT and 9 EμMyc;Prdm11 KO end-stage splenic tumors

2015-03-02 | E-GEOD-56063 | biostudies-arrayexpress

PRDM11 ChIP in U2932 cells

Project description:The PR-domain family e(PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We found that loss of Prdm11 accelerates MYC-driven lymphomagenesis in the Eµ-Myc mouse model. Moreover, we show that patients with PRDM11-deficient diffuse large B cell lymphomas (DLBCLs) have poorer overall survival and belong to the non-Germinal Center B cell (GCB)-like subtype. Mechanistically, genome-wide mapping of PRDM11 binding sites coupled with transcriptome sequencing in human DLBCL cells evidenced that PRDM11 associates with transcriptional start sites of target genes and regulates important oncogenes such as FOS and JUN. Hence, we characterize PRDM11 as a novel tumor suppressor controlling the expression of key oncogenes and add new mechanistic insight into B-cell lymphomagenesis. 5 samples: PRDM11 Ab1, PRDM11 Ab2, RNA Polymerase II, IgG and input

2015-03-02 | E-GEOD-56064 | biostudies-arrayexpress

The proteomic changes of GES1 infected by Helicobacter pylori

Project description:We explored the proteomic changes in GES1 cells induced by H.pylori. GES1 cells cocultured with increasing concentrations of H.pylori were subjected to quantitative proteomic analyses using label-free methods for relative quantitation.

2022-02-14 | PXD025281 | Pride

A mouse model of the most aggressive subgroup of human medulloblastoma [HT_MG-430_PM]

Project description:A series of mouse models designed to mimic pediatric medulloblastoma types in humans were tested by microarray and compared to published human medulloblastoma data Myc-type tumors [dka201-203] were generated by orthotopic injection of Myc-infected cerebellar cells from Cdkn2c-/-, Trp53-/-, Atoh1-GFP mice into the cerebral cortex of immunocompromised nude mice. For Shh-type medulloblastomas [dka204-206], spontaneous medulloblastomas from [Cdkn2c-/-; Trp53Fl/Fl; Nestin-Cre] (Uziel et al.,2005 Genes Dev) were used. FACS-sorted GFP-positive [dka220-222] and GFP-negative [dka211, 212 and 219] populations were obtained from postnatal day 6 Cdkn2c-/-, Trp53-/-, Atoh1-GFP cerebella. Myc-type secondary tumors [dka223-225] were generated by orthotopic transplantation of cultured sphere cells from Myc-type primary tumors.

2012-02-29 | E-GEOD-33200 | biostudies-arrayexpress

A mouse model of the most aggressive subgroup of human medulloblastoma

Project description:This SuperSeries is composed of the following subset Series: GSE33199: A mouse model of the most aggressive subgroup of human medulloblastoma [Mouse430_2] GSE33200: A mouse model of the most aggressive subgroup of human medulloblastoma [HT_MG-430_PM] Refer to individual Series

2012-02-29 | E-GEOD-33201 | biostudies-arrayexpress

MMTV-Myc tumor development in E2F-null backgrounds

Project description:Advances in genomic signatures have begun to dissect breast cancer heterogeneity, and application of these signatures will allow the prediction of which pathways are important in tumor development. Here we used genomic signatures to predict involvement of specific E2F transcription factors in Myc-induced tumors. We genetically tested this prediction by interbreeding Myc transgenics with mice lacking various activator E2F alleles. Tumor latency decreased in the E2F1 mutant background and significantly increased in both the E2F2 and E2F3 mutants. Investigating the mechanism behind these changes revealed a reduction in apoptosis in the E2F1 knockout strain. E2F2 and E2F3 mutant backgrounds alleviated Myc effects on the mammary gland, reducing the susceptible tumor target population. Gene expression data from tumors revealed that the E2F2 knockout background resulted in fewer tumors with EMT, corresponding with a reduction in probability of Ras activation. In human breast cancer we found that a low probability of E2F2 pathway activation was associated with increased relapse-free survival time. Together these data illustrate the predictive utility of genomic signatures in deciphering the heterogeneity within breast cancer and illustrate the unique genetic requirements for individual E2Fs in mediating tumorigenesis in both mouse models and human breast cancer. MMTV-Myc tumors were generated in an E2F wild-type, E2F1 null, E2F2 null and E2F3 heterozygous background. When the primary tumor reached the endpoint, the tumors were flash frozen. 20 tumors from each genotype were selected for microarray analysis.

2011-12-29 | E-GEOD-24594 | biostudies-arrayexpress

Increased metastasis with loss of E2F2 in Myc-driven tumors

Project description:In human breast cancer, mortality is associated with metastasis to distant sites. Therefore, it is critical to elucidate the biological mechanisms that underlie tumor progression and metastasis. Using signaling pathway signatures we previously predicted a role for E2F transcription factors in Myc induced tumors. To test this role we interbred MMTV-Myc transgenic mice with E2F knockouts. Surprisingly, we observed that the loss of E2F2 sharply increased the percentage of lung metastasis in MMTV-Myc transgenic mice. Examining the gene expression profile from these tumors, we identified genetic components that were potentially involved in mediating metastasis. These genes were filtered to uncover the genes involved in metastasis that also impacted distant metastasis free survival in human breast cancer. In order to elucidate the mechanism by which E2F2 loss enhanced metastasis we generated knockdowns of E2F2 in MDA-MB-231 cells and observed increased migration in vitro and increased lung colonization in vivo. We then examined genes that were differentially regulated between tumors from MMTV-Myc, MMTV-Myc E2F2-/-, and lung metastases samples and identified PTPRD. To test the role of PTPRD in E2F2-mediated breast cancer metastasis, we generated a knockdown of PTPRD in MDA-MB-231 cells. We noted that decreased levels of PTPRD resulted in decreased migration in vitro and decreased lung colonization in vivo. Taken together, these data indicate that E2F2 loss results in increased metastasis in breast cancer, potentially functioning through a PTPRD dependent mechanism. Lung metastases from MMTV-Myc tumors in a E2F2 knockout and E2F3 +/- backgrounds were analyzed for their gene expression profile

2016-08-08 | E-GEOD-71815 | biostudies-arrayexpress

Nuclear Factor I/B is an Oncogene in Small Cell Lung Cancer

Project description:Small cell lung cancer (SCLC) is an aggressive cancer often diagnosed only after it has metastasized to distant sites (Meuwissen and Berns 2005; Cooper and Spiro 2006). Despite the need to better understand this disease, SCLC remains poorly characterized at the molecular and genomic levels (Forgacs et al. 2001; Pleasance et al. 2010). Using a genetically-engineered mouse model of SCLC driven by conditional deletion of Trp53 and Rb1 in the lung (Jonkers et al. 2001; Vooijs et al. 2002; Meuwissen et al. 2003; Sage et al. 2003), we identified several frequent, high-magnitude focal DNA copy number alterations in SCLC. We uncovered amplification of a novel, oncogenic transcription factor, Nuclear Factor I/B (Nfib) in the mouse SCLC model and in human SCLC. Functional studies indicate that NFIB regulates cell viability and proliferation during transformation. Gene expression analysis of two replicates each of two independent mSCLC cell lines (3583T3 and 3151T4) stably expressing Nfib, Mycl1 or both Nfib and Mycl1

2011-12-08 | E-GEOD-29533 | biostudies-arrayexpress

Single-cell characterization of anti-LAG3+anti-PD1 treatment in melanoma patients

Project description:We evaluated blood samples from 6 patients with metastatic melanoma treated with anti-LAG3+anti-PD1 (160+480 mg) in a phase I trial (NCT01968109) using single-cell RNA and T cell receptor (TCR) sequencing (scRNA+TCRαβ-seq, 10X 5') combined with other multiomics profiling (flow, cytokine, TCRb-seq) from a larger cohort of 40 patients. This data set include three time points, including baseline, 1 month, and 3 month. The sorting is CD45+.

2023-02-03 | E-MTAB-12733 | biostudies-arrayexpress

Top2a identifies and provides epigenetic rationale for novel combination therapeutic strategies for aggressive prostate cancer

Project description:We perform RNA-seq on matched orthotopic murine primary and metastatic prostate cancer samples to identify differential gene expressions RNA-seq was performed on orthotopic murine primary and metastatic tumor samples using Illumina Hi-Seq 2000 platform

2015-01-30 | E-GEOD-64771 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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