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Expression data from Eµ-Myc B-cell lymphoma

ABSTRACT: We used microarrays to understand gene expression changes in response to DNA crosslinking agent mafosfamide over a 48 hour period. We also created resistant cell lines (R100, R500, R1000, R2000, R4000) via dose escalation and used microarrays to probe expression changes between the parental and resistant cell lines.

ORGANISM(S): Mus musculus

PROVIDER: GSE60342 | GEO | 2014/08/13

SECONDARY ACCESSION(S): PRJNA258063

REPOSITORIES: GEO

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Expression data from EÂµ-Myc B-cell lymphoma

Project description:We used microarrays to understand gene expression changes in response to DNA crosslinking agent mafosfamide over a 48 hour period. We also created resistant cell lines (R100, R500, R1000, R2000, R4000) via dose escalation and used microarrays to probe expression changes between the parental and resistant cell lines. EÂµ-Myc B-cells were co-cultured in vitro with 750nM mafosfamide for 48 hours. Samples were collected at 0, 6, 12, 24, and 48 hours. Additionally, resistant lines were either treated or untreated with 750nM for 24 hours.

2014-08-13 | E-GEOD-60342 | biostudies-arrayexpress

Epigenetic Analysis of Eµ-Myc B-cell lymphoma using both H3K27me3 CHiP-Seq and Bisulfite-Seq (reduced representation).

Project description:We used RRBS and H3K27me3 to understand epigenetic changes in resistant cell lines to DNA crosslinking agent, mafosfamide, (Parental, R100, R500, R1000, R2000, R4000) via dose escalation.

2016-03-08 | GSE78939 | GEO

Anti-apoptotic A1 is not essential for lymphoma development in Eµ-Myc mice but helps sustain transplanted Eµ-Myc tumour cells.

Project description:The transcription factor c-MYC regulates a multiplicity of genes involved in cellular growth, proliferation, metabolism and DNA damage response and its overexpression is a hallmark of many tumours. Since MYC promotes apoptosis under conditions of stress, such as limited availability of nutrients or cytokines, MYC-driven cells are very much dependent on signals that inhibit cell death. Stress signals trigger apoptosis via the pathway regulated by opposing fractions of the BCL-2 protein family and previous genetic studies have shown that the development of B lymphoid tumours in Eµ-Myc mice is critically dependent on expression of pro-survival BCL-2 relatives MCL-1, BCL-W and, to a lesser extent, BCL-XL, but not BCL-2 itself, and that sustained growth of these lymphomas is dependent on MCL-1. Using recently developed mice that lack expression of all three functional pro-survival A1 genes, we show here that the kinetics of lymphoma development in Eµ-Myc mice and the competitive repopulation capacity of Eµ-Myc haemopoietic stem and progenitor cells is unaffected by the absence of A1. However, conditional loss of a single remaining functional A1 gene from transplanted A1-a-/-A1-b fl/fl A1-c-/- Eµ-Myc lymphomas slowed their expansion, significantly extending the life of the transplant recipients. Thus, A1 contributes to the survival of malignant Eµ-Myc-driven B lymphoid cells. These results strengthen the case for BFL-1, the human homologue of A1, being a valid target for drug development for MYC-driven tumours.

| S-EPMC5864240 | biostudies-literature

Addiction to Runx1 is partially attenuated by loss of p53 in the Eµ-Myc lymphoma model.

Project description:The Runx genes function as dominant oncogenes that collaborate potently with Myc or loss of p53 to induce lymphoma when over-expressed. Here we examined the requirement for basal Runx1 activity for tumor maintenance in the Eµ-Myc model of Burkitt's lymphoma. While normal Runx1fl/fl lymphoid cells permit mono-allelic deletion, primary Eµ-Myc lymphomas showed selection for retention of both alleles and attempts to enforce deletion in vivo led to compensatory expansion of p53null blasts retaining Runx1. Surprisingly, Runx1 could be excised completely from established Eµ-Myc lymphoma cell lines in vitro without obvious effects on cell phenotype. Established lines lacked functional p53, and were sensitive to death induced by introduction of a temperature-sensitive p53 (Val135) allele. Transcriptome analysis of Runx1-deleted cells revealed a gene signature associated with lymphoid proliferation, survival and differentiation, and included strong de-repression of recombination-activating (Rag) genes, an observation that was mirrored in a panel of human acute leukemias where RUNX1 and RAG1,2 mRNA expression were negatively correlated. Notably, despite their continued growth and tumorigenic potential, Runx1null lymphoma cells displayed impaired proliferation and markedly increased sensitivity to DNA damage and dexamethasone-induced apoptosis, validating Runx1 function as a potential therapeutic target in Myc-driven lymphomas regardless of their p53 status.

| S-EPMC5029604 | biostudies-literature

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 [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 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

Transgenic Eµ-myc mouse lymphoma array CGH data

Project description: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.

2014-09-10 | GSE40759 | GEO

Transgenic Eµ-myc mouse lymphoma array CGH data

Project description: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.

2014-09-10 | E-GEOD-40759 | biostudies-arrayexpress

<i>Max</i> deletion destabilizes MYC protein and abrogates Eµ-<i>Myc</i> lymphomagenesis.

Project description:Although MAX is regarded as an obligate dimerization partner for MYC, its function in normal development and neoplasia is poorly defined. We show that B-cell-specific deletion of Max has a modest effect on B-cell development but completely abrogates Eµ-Myc-driven lymphomagenesis. While Max loss affects only a few hundred genes in normal B cells, it leads to the global down-regulation of Myc-activated genes in premalignant Eµ-Myc cells. We show that the balance between MYC-MAX and MNT-MAX interactions in B cells shifts in premalignant B cells toward a MYC-driven transcriptional program. Moreover, we found that MAX loss leads to a significant reduction in MYC protein levels and down-regulation of direct transcriptional targets, including regulators of MYC stability. This phenomenon is also observed in multiple cell lines treated with MYC-MAX dimerization inhibitors. Our work uncovers a layer of Myc autoregulation critical for lymphomagenesis yet partly dispensable for normal development.

| S-EPMC6719623 | biostudies-literature

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