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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Anders Lund

PROVIDER: E-GEOD-56063 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

2015-03-02 | GSE56063 | GEO

PRDM11: a novel tumor suppressor

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

2015-03-02 | E-GEOD-56065 | 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.

2015-03-02 | GSE56064 | GEO

PRDM11 ChIP in U2932 cells

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

Effect of PRDM11 depletion in U2932 cells

2015-03-02 | GSE56235 | GEO

Effect of PRDM11 depletion in U2932 cells

2015-03-02 | E-GEOD-56235 | biostudies-arrayexpress

Transcription profiling of mouseB-cell lymphomas with defined genetic alterations in p53 or p73

Project description:Induction of apoptosis by the tumor suppressor p53 is known to protect from Myc-driven lymphomagenesis. The p53 family member p73 is also a pro-apoptotic protein, which is activated in response to oncogenes like Myc. We therefore investigated whether p73 provides a similar protection from Myc-driven lymphomas as p53. To generate B-cell lymphomas with defined genetic alterations in p53 or p73, we crossed the Eµ-Myc transgenic to mice heterozygous for germ-line deletions in p53 (p53+/) or p73 (p73+/-). Lymphomas which have spontaneously developed in Eµ-Myc transgenic animals with the genotypes p53+/+, p53+/-, p73+/+, p73+/- or p73-/- were isolated when the animals were moribund and further processed for gene expression profiling with 22.5K cDNA microarrays.

2008-12-05 | E-MEXP-1620 | biostudies-arrayexpress

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

Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (ChIP-Seq)

Project description:Constitutively active MYC and reactivated telomerase often co-exist in cancers. While the reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with co-factors, confers several growth advantages to cancer cells. However, it is unclear which co-factors sustain elevated MYC activity in tumours . Here, we identify TERT, the catalytic subunit of telomerase, as a novel regulator of MYC stability in cancers. Binding of TERT to MYC stabilizes its levels on chromatin, contributing to either activation or repression of its target genes. Mechanistically, TERT regulates MYC ubiquitination and stability, and this effect of TERT is independent of its role on telomeres. Genetic inhibition and knocking out of TERT phenocopied the loss of MYC, resulting in reduced disease burden of early- and late-stage MYC-driven murine lymphomas. Conversly, the ectopic expression of TERT could substitute for reduced MYC in these functions. Finally we show that TERT null mice, unlike Terc null mice, show delayed onset of MYC induced lymphomagenesis. Accordingly, inhibiting TERT function in primary human leukemia cells blocked the expression of MYC targets, while Terc depletion had no effects . Based on our data, we conclude that the re-expression of TERT, a direct MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis. ChIP was performed using anti-MYC (sc-764) in primary lymphoma cells from Eµ-Myc;Tert -/- mice, Eµ-Myc;Tert +/+ mice, or in P493 cells treated with shTert, P493 shTerc and shControl.

2015-04-23 | E-GEOD-60223 | 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

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