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Gene Expression profiling of Myc-induced lymphomagenesis

ABSTRACT: The ability of oncogenes to provoke cancer is harnessed by regulators that control cell proliferation or induce apoptosis, and bypass of these checkpoints is a hallmark of malignancies. Myc oncoproteins are overexpressed in ~70% of all cancers and induce numerous transcription targets that regulate cell growth, metabolism, and the ribosome machinery. We used the Eμ-Myc mouse model from which one can directly compare expression profiles of wild type versus Myc-expressing B220+ pre-malignant lymphocytes and also queried differences in gene expression that ensue following the neoplastic switch to lymphoma (Nilsson et al., 2005 - PMID:15894264 and Keller et al. 2010 - PMID:20598117).

ORGANISM(S): Mus musculus

PROVIDER: GSE32239 | GEO | 2011/10/31

SECONDARY ACCESSION(S): PRJNA147195

REPOSITORIES: GEO

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Gene Expression profiling of Myc-induced lymphomagenesis

Project description:The ability of oncogenes to provoke cancer is harnessed by regulators that control cell proliferation or induce apoptosis, and bypass of these checkpoints is a hallmark of malignancies. Myc oncoproteins are overexpressed in ~70% of all cancers and induce numerous transcription targets that regulate cell growth, metabolism, and the ribosome machinery. We used the Eμ-Myc mouse model from which one can directly compare expression profiles of wild type versus Myc-expressing B220+ pre-malignant lymphocytes and also queried differences in gene expression that ensue following the neoplastic switch to lymphoma (Nilsson et al., 2005 - PMID:15894264 and Keller et al. 2010 - PMID:20598117). Wild type and precancerous Eμ-Myc transgenic B cells (from 4-6 week old littermates), and lymphomas from 13 independent Eμ-Myc mice were investigated. These samples were used for subsequent RNA purification, labeling and hybridization to MOE430A Affymetrix arrays.

2011-10-31 | E-GEOD-32239 | biostudies-arrayexpress

DNMT3B7 disrupts embryonic development and accelerates lymphomagenesis

Project description:Cancer cells have an altered distribution of DNA methylation and express aberrant DNA methyltransferase 3B transcripts, which encode truncated proteins. To test if a truncated DNMT3B isoform disrupts DNA methylation in vivo, we constructed transgenic mice expressing DNMT3B7, a common truncated DNMT3B isoform in cancer cells. DNMT3B7 transgenic mice exhibit altered embryonic development, including lymphopenia, craniofacial abnormalities, and cardiac defects, similar to Dnmt3b-deficient animals, but rarely develop cancer. However, DNMT3B7 expression increases the frequency of mediastinal lymphomas in Eμ−myc animals. Eμ-myc/DNMT3B7 lymphomas have more chromosomal rearrangements, increased global methylation levels, and more locus-specific perturbations in DNA methylation patterns compared to Eμ-myc lymphomas. Our results demonstrate that a truncated DNMT3B protein can alter tumorigenesis, suggesting a similar role in human tumors. Direct comparison of DNA methylation in lymphoma samples from Eu-Myc vs Eu-Myc/Dnmt3b7 mice.

2010-07-30 | E-GEOD-21273 | biostudies-arrayexpress

Positive and negative regulation of lymphomagenesis by the NF-kappaB subunit c-Rel

Project description:'The REL gene, encoding the NF-κB subunit c-Rel, is frequently amplified in B-cell lymphoma and functions as a tumour promoting transcription factor. Here we report the surprising result that c-rel -/- mice display significantly earlier lymphomagenesis in the c-Myc driven, Eμ-Myc model of B-cell lymphoma. c-Rel loss also led to earlier onset of disease in a separate TCL1-Tg driven lymphoma model. Tumour reimplantation experiments indicated that this is an effect intrinsic to the Eμ-Myc lymphoma cells but, counter-intuitively, c-rel -/- Eμ-Myc lymphoma cells were more sensitive to apoptotic stimuli. To learn more about why loss of c-Rel led to earlier onset of disease, microarray gene expression analysis was performed on B-cells from 4-week old, wild type and c-rel -/- Eμ-Myc mice. Extensive changes in gene expression were not seen at this age but among those transcripts significantly downregulated by the loss of c-Rel was the B-cell tumour suppressor BTB and CNC homology 2 (Bach2). Q-PCR and western blot analysis confirmed loss of Bach2 in c-Rel mutant Eμ-Myc tumours at both 4 weeks and the terminal stages of disease. Moreover Bach2 expression was also downregulated in c-rel -/- TCL1-Tg mice and RelA Thr505Ala mutant Eμ-Myc mice. Analysis of wild type Eμ-Myc mice demonstrated that the population expressing low levels of Bach2 exhibited the earlier onset of lymphoma seen in c-rel-/- mice. Confirming the relevance of these findings to human disease, analysis of ChIP-Seq data revealed that Bach2 is a c-Rel and NF-κB target gene in transformed human B-cells, while treatment of Burkitt''s lymphoma cells with inhibitors of the NF-κB/IKK pathway or deletion of c-Rel or RelA resulted in loss of Bach2 expression. This data reveals a surprising tumour suppressor role for c-Rel in lymphoma development explained by regulation of Bach2 expression, underlining the context dependent complexity of NF-κB signalling in cancer.'

2014-12-31 | E-MTAB-2774 | biostudies-arrayexpress

DNMT3B7 disrupts embryonic development and accelerates lymphomagenesis

2010-07-30 | GSE21273 | GEO

IL-6 promotes MYC-induced B cell lymphomagenesis independent of STAT3

Project description:The inflammatory cytokine IL-6 is known to play a causal role in the promotion of cancer, although the underlying mechanisms remain to be completely understood. Interplay between endogenous and environmental cues determines the fate of cancer development. The Eμ-myc transgenic mouse expresses elevated levels of c-Myc in the B cell lineage and develops B cell lymphomas with associated mutations in p53 or other genes linked to apoptosis. We generated Eμ-myc mice that either lacked the IL-6 gene, or lacked the STAT3 gene specifically in B cells to determine the role of the IL-6/JAK/STAT3 pathway in tumor development. Using the Eμ-myc lymphoma mouse model, we demonstrate that IL-6 is a critical tumor promoter during early stages of B cell lymphomagenesis. IL-6 is shown to inhibit the expression of tumor suppressors, notably BIM and PTEN, thereby advancing MYC-driven B cell tumorigenesis. Several miRNAs known to target BIM and PTEN are upregulated by IL-6 and likely lead to the stable suppression of pro-apoptotic pathways early during the tumorigenic process. STAT3, a classical downstream effector of IL-6, appears dispensable for Eμ-myc driven lymphomagenesis. We conclude that the growth-promoting and anti-apoptotic mechanisms activated by IL-6 are critically involved in Eμ-myc driven tumor initiation and progression, but the B cell intrinsic expression of STAT3 is not required.

2021-02-02 | GSE165205 | GEO

Osteoblastic loss of Ezh2

Project description:Osteblastic loss of Ezh2 was achieved by breeding Ezh2flox/flox (Su et al., PMID: 12496962) with Osx-Cre (Rodda et al., PMID:16854976).

2018-07-25 | GSE111245 | GEO

rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [4C-seq]

Project description:Long-range interactions of ribososomal DNA (rDNA) identified by 4C-seq in mouse wildtype, premalignant and malignant Eμ-Myc cells and tissue culture adapated Eμ-Myc-shUbtf and Eμ-Myc-LMP (empty vector) cells.

2019-02-06 | GSE70221 | GEO

Effect of NEK2 deficiency on gene expression of CD19-selected spleen B cells of Eμ-myc mouse model

Project description:NEK2 overexpression in the B cell lineage affects B cell development. To determine whether deficiency of NEK2 inhibits B cell malignancies, we crossed Nek2 knockout mice with Eμ-myc transgenic mice, a well-established Myc-driven preclinical model for B cell malignancies. Three genotyping offsprings were obtained: Eμ-myc/Nek2+/+ (NEK2 wild type), Eμ-myc/Nek2+/- (NEK2 heterozygotes), and Eμ-myc/Nek2-/- (NEK2 homozygotes). Bulk RNA-seq was performed on CD19-selected spleen B cells to view the transcriptome differences.

2023-06-01 | GSE226675 | GEO

SeaIce, Espegrend, Microscosm, Mnemi

Project description:454 dataset for Hosia, et al. Torstensson et al. Dinasquet et al.

| PRJEB7907 | ENA

Differential gene expression of meiotic drive system of Aedes aegypti

Project description:We conducted a whole transcriptome analysis of testes from a meiotic drive-carrying strain (T37) in comparison with a drive-sensitive strain (RED) using microarrays based on the complete annotated Ae. aegypti gene set. The T37 strain, which carries a strong meiotic drive gene (Mori et al., 2004 (PMID 15605641)), was established from mosquitoes collected in Trinidad. The RED strain is highly sensitive to the meiotic drive gene (Hickey and Craig, 1966 (PMID ); Mori et al., 2004 (PMID 15605641)).

2015-07-15 | GSE43562 | GEO

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