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Expression data from primary mouse Emu-myc B-cell lymphoma.

ABSTRACT: We are interested in genetic programs and mutations which impact on tumor development and sensitivity to anticancer therapies. Utilizing Emu-myc transgenic mice, which spontaneously develop aggressive B-cell lymphomas, we aimed here to study the effects of drug responses in vivo. For that purpose, primary lymphomas from the Emu-myc transgenic mice were transplanted in several immunocompetent recipients and exposed to a single dose Cyclophosphamide (CTX), a standard component of chemotherapeutic regimens used to treat human B-cell lymphomas. Approximately one half of recipient mice are cured with this treatment (Never Relapse Lymphomas, NR), while in other half lymphomas relapse over time (Relapse Prone Lymphomas, RP), allowing us to treat these relapsed mice with progressively shorter durations of remission into full-blown clinical resistance (Resistant Lymphomas, RES). Looking at the differences between NR, RP and RES lymphomas, each in therapy-naive state or after drug challenge, we aimed here to decipher the genetic and biochemical components determining the susceptibility of lymphoma cells to respond to standard chemotherapeutic drugs.

ORGANISM(S): Mus musculus

PROVIDER: GSE134751 | GEO | 2020/03/19

REPOSITORIES: GEO

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Expression data from primary mouse Emu-myc B-cell lymphoma

Project description:We are interested in genetic programs and mutations which impact on tumor development and sensitivity to anticancer therapies. Utilizing Emu-myc transgenic mice, which spontaneously develop aggressive B-cell lymphomas, we aimed here to study the effects of drug responses in vivo, in particular genetic and biochemical components presented a priori in therapy-naive tumor cells, which determine the susceptibility of lymphoma cells to respond to standard chemotherapeutic drugs. We used global gene expression profiling by microarrays to gain insight into the molecular program underlying the chemotherapy response potential in primary Emu-myc transgenic B-cell lymphomas.

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Identification of PRDM15 Cistrome in Emu-Myc Lymphoma cells

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Expression data from Adriamycin-treated Emu-myc; Suv39h1-/- B-cell lymphoma

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Expression data from treatment-induced senescence in mouse Emu-myc B-cell lymphoma model

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2016-07-22 | E-GEOD-49356 | biostudies-arrayexpress

Transcriptome of hematopoietic stem cells from wild-type and Eumyc transgenic mice on wild-type or caspase-1/11 double knockout backgrounds

Project description:To determine the transcriptional effects of caspase 1 and caspase 11 deficiency as well as Emu-myc, we performed RNA sequencing (RNAseq) on sorted HSCs from four groups of mice (wild type, Emu-myc, Casp1−⁄−Casp11−⁄−, and Casp1−⁄−Casp11−⁄−Emu-myc).

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Comprehensive Study of Nuclear Receptor DNA Binding Provides a Revised Framework for Understanding Receptor Specificity

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Transcription profiling of mouse multiple myeloma tumors and splenic B cells from transgenics overexpressing XBP-1s

Project description:Multiple myeloma (MM) evolves from highly prevalent premalignant condition termed Monoclonal Gammopathy of Undetermined Significance (MGUS). We report an MGUS-MM phenotype arising in transgenic mice with Emu-directed expression of the unfolded protein/ER stress response and plasma cell development spliced isoform factor XBP-1s. Emu-XBP-1s elicited elevated serum Ig and IL-6 levels, skin alterations and with advancing age, a significant proportion of Emu-xbp-1s transgenic mice develop features diagnostic of human MM including bone lytic lesions. Transcriptional profiles of Emu-xbp-1s B lymphoid and MM cells show aberrant expression of genes known to be dysregulated in human MM including Cyclin D1, MAF, MAFB, and APRIL. This genetic model coupled with documented frequent XBP-1s overexpression in human MM serve to implicate chronic XBP-1s dysregulation in the development of this common and lethal malignancy. Experiment Overall Design: In this study, we have explored the biological impact of sustained XBP-1s expression in the lymphoid system, anticipating that this genetic event would be a necessary component along with other MM-relevant oncogenes and tumor suppressor gene manipulations to generate a MM-prone mouse model. Unexpectedly, XBP-1s overexpression alone yielded an MGUS-MM disease bearing many features classical of the human disease on the clinical, pathological and molecular levels. Experiment Overall Design: We performed expression analysis of B cells derived from the spleen of 20-week old Emu-xbp-1s mice (n=5) and non-transgenic mice (n=5). Additionally, we analyzed the expression profiles from MM tumor cells arising in Emu-xbp-1s mice (n=6).

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RNA-seq analysis of pro-B cells from RAG, double RAG/Emu, double RAG/3'RR and double RAG/KOKI deficient mice.

Project description:By their impact on nuclear organisation, enhancers are master regulators of cell fate. We thus developed double Emu-RAG-deficient, 3’RR-RAG-deficient mice and KOKI-RAG-deficient mice to investigate a potential transcriptional cross-talk between Emu and 3'RR enhancers at the pro-B cell stage.

2019-02-07 | GSE117449 | GEO

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