Transcriptional changes thymic lymphomas with overexpression of mutant MYC
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA798708 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17662827.fastq.gz | Fastqsanger.gz | |||
| SRR17662828.fastq.gz | Fastqsanger.gz | |||
| SRR17662829.fastq.gz | Fastqsanger.gz | |||
| SRR17662830.fastq.gz | Fastqsanger.gz | |||
| SRR17662831.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:The goal of this study was to determine gene expression changes in thymic lymphomas with overexpression of mutant MYC
2022-07-14 | GSE193995 | GEO
Project description:RNA sequencing of Mus musculus thymic lymphomas
2019-06-06 | GSE85894 | GEO
Project description:RNA sequencing of Mus musculus thymic lymphomas
2020-12-30 | GSE121739 | GEO
Project description:This dataset comprises expression profiles from 3 thymic lymphomas from Ikaros deficient mice (IkL/L model, see Dumortier et al, Mol. Cell. Biol. 26, 209-220, 2006 for a description of the tumor model) and 3 thymic lymphomas from IkL/L mice that harbor a mutation of the Notch1 gene (deletion of floxed sequences comprising the promoter and exon 1 with the CD4-Cre transgene). The results from this experimpent is that the expression of Notch target genes was unexpectedly not altered in the tumors with the Notch1 deletion. This result is explained by the activation of a cryptic 3' Notch1 promoter in the deleted tumors, which leads to constitutive Notch1 activation. These results are described in the following publication: R Jeannet, J Mastio, B Macias-Garcia, A Oravecz, T Ashworth, AS Geimer-Lelay, B Jost, S Le Gras, J Ghysdael, T Gridley, T Honjo, F Radtke, J Aster, S Chan and P Kastner. Oncogenic activation of the Notch1 gene in mouse T-cell leukemia by deletion of its promoter. Blood, in press (2010) Primary thymic tumors from 3 IkL/L Notch1+/+ CD4-Cre+ mice (aged 18-20 weeks) were compared to similar tumors from 3 IkL/L Notch1f/f CD4-Cre+ mice (aged 8-10 weeks).
2010-09-03 | E-GEOD-23972 | biostudies-arrayexpress
Project description:Expression profiling of thymic lymphomas derived from HIF1a+/+, p53R270H/R270H; HIF1a+/-, p53R270H/R270H; and HIF1aKI/+, p53R270H/R270H mice. HIF1a and HIF2a share a high degree of sequence homology, but recent work has shown that the two a subunits can have contrasting and tissue-specific effects on tumor growth. To directly compare the role of each HIFa subunit in spontaneous tumorigenesis, we bred a mouse model of expanded HIF2a expression and Hif1a+/- mice to homozygotes for the R270H mutation in p53. Heterozygosity for Hif1a significantly reduced the incidence of thymic lymphomas observed in this model. Moreover, reduced Hif1a levels correlated with decreased stabilization of activated Notch1 and expression of the Notch target genes, Dtx1 and Nrarp. Keywords: genetic modification, disease state analysis
2009-01-12 | GSE14336 | GEO
Project description:Expression profiling of thymic lymphomas derived from HIF1a+/+, p53R270H/R270H; HIF1a+/-, p53R270H/R270H; and HIF1aKI/+, p53R270H/R270H mice. HIF1a and HIF2a share a high degree of sequence homology, but recent work has shown that the two a subunits can have contrasting and tissue-specific effects on tumor growth. To directly compare the role of each HIFa subunit in spontaneous tumorigenesis, we bred a mouse model of expanded HIF2a expression and Hif1a+/- mice to homozygotes for the R270H mutation in p53. Heterozygosity for Hif1a significantly reduced the incidence of thymic lymphomas observed in this model. Moreover, reduced Hif1a levels correlated with decreased stabilization of activated Notch1 and expression of the Notch target genes, Dtx1 and Nrarp. Keywords: genetic modification, disease state analysis Thymic lymphoma tissue was preserved at the time mice were sacrificed. 4-5 samples from each of 3 genotypes (HIF1a+/-, p53R270H/R270H, HIF1aKI/+; p53R270H/R270H; and HIF1a+/+, p53R270H/R270H) were then used for microarray analysis to identify differences in gene expression that could account for changes in tumor onset and incidence.
2009-01-12 | E-GEOD-14336 | biostudies-arrayexpress
Project description:The suppression of oncogenic levels of MYC is sufficient to induce sustained tumor regression associated with proliferative arrest, differentiation, cellular senescence and/or apoptosis, a phenomenon known as oncogene addiction. However, after prolonged inactivation of MYC in a conditional transgenic mouse model of Em-tTA/tetO-MYC T-acute lymphomablastic lymphoma (T-ALL), some of the tumors recur, recapitulating what is frequently observed in human tumors in response to targeted therapies. Here we report that these recurring lymphomas express high levels of either transgenic or endogenous Myc suggesting that tumors continue to be addicted to oncogenic levels of MYC. Many of the recurring lymphomas (76%) harbored mutations in the tetracycline transactivator (tTA) resulting in expression of the MYC transgene even in the presence of doxycycline. Many of the remaining recurring tumors expressed high levels of endogenous Myc which was in some cases associated with a genomic rearrangement of the endogenous Myc locus or overexpression of Notch1. Gene expression profiling confirmed that the primary and recurring tumors have highly similar transcriptomes. Importantly, shRNA-mediated suppression of the high levels of MYC in recurring tumors elicited both suppression of proliferation and increased apoptosis confirming that these tumors remain oncogene addicted. These results suggest that tumors caused by MYC overexpression remain addicted to high levels of expression of this oncogene. 13 samples, no replicates included
2011-09-23 | E-GEOD-32341 | biostudies-arrayexpress
Project description:Amino acid levels analysis of lymphomas isolated from Eu-Myc;CD19-Cre;Odc fl/fl mic and their wild-type counterparts Eu-Myc;CD19-Cre;Odc +/+
2016-09-08 | ST000461 | MetabolomicsWorkbench
Project description:Lck-MyrAkt2 mice develop spontaneous thymic lymphomas at approximately 100-200 days of age, driven in part by a consitutatively-active AKT (due to myristoylation). mTOR Knock Down mice were crossed with Lck-MyrAkt postive mice to model the affects of decreasing mTOR activity on tumors with an activated PI3K/AKT/MTOR pathway. Lck-Akt/mTOR KD mice had prolonged survival compared to the Lck-Akt/mTOR WT mice. We used microarrays to compare the transcriptome in thymic lymphomas between Lck-Akt positive, mTOR WT and Lck-Akt positive, mTOR KD mice. Four thymic lymphomas from Lck-Akt/mTOR WT mice were compared to three thymic lymphomas from Lck-Akt/mTOR KD mice.
2015-09-15 | E-MTAB-3242 | biostudies-arrayexpress
Project description:This dataset comprises expression profiles from 3 thymic lymphomas from Ikaros deficient mice (IkL/L model, see Dumortier et al, Mol. Cell. Biol. 26, 209-220, 2006 for a description of the tumor model) and 3 thymic lymphomas from IkL/L mice that harbor a mutation of the Notch1 gene (deletion of floxed sequences comprising the promoter and exon 1 with the CD4-Cre transgene). The results from this experimpent is that the expression of Notch target genes was unexpectedly not altered in the tumors with the Notch1 deletion. This result is explained by the activation of a cryptic 3' Notch1 promoter in the deleted tumors, which leads to constitutive Notch1 activation. These results are described in the following publication: R Jeannet, J Mastio, B Macias-Garcia, A Oravecz, T Ashworth, AS Geimer-Lelay, B Jost, S Le Gras, J Ghysdael, T Gridley, T Honjo, F Radtke, J Aster, S Chan and P Kastner. Oncogenic activation of the Notch1 gene in mouse T-cell leukemia by deletion of its promoter. Blood, in press (2010)
2010-09-03 | GSE23972 | GEO