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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.

2020-12-31 | GSE38428 | GEO

Transcriptome analysis of B cell lymphomas in several c-myc Igh transgenic mice

Project description:Investigation of B cell lymphomas (IgM+ IgD+) located in various places (lung, mesenteric lymph nodes,…) of three different c-myc Igh transgenic mice. Insertion of c-myc in 5' to Emu (cr), in 5' to Cmu with Emu deletion (hv), and in Calpha (co).

2020-01-21 | GSE132721 | GEO

Identification of PRDM15 Cistrome in Emu-Myc Lymphoma cells

Project description:Genome-wide binding targets of PRDM15 were identified in Emu-Myc Lymphomas

2019-07-04 | GSE116905 | GEO

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

Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc; Suv39h1-/- mice were used. In this model, the c-Myc oncogene is constitutively expressed in the cells of the B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas. Adriamycin (ADR), a cytostatic drug used as a standard part of several lymphoma treatment regimens, is known to massively induce TIS in Suv39h1-proficient lymphomas, protected from apoptosis by Bcl-2 over expression (Myc;Bcl2). In order to discern the impact of Suv39h1 to TIS induction under these conditions, we analysed here transcriptional profiles of matched pairs of Emu-myc;Suv39h1-/-;Bcl2 lymphomas, untreated or treated for 5 days with ADR.

2013-07-04 | E-GEOD-44355 | biostudies-arrayexpress

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

Project description:Treatment induced senescence (TIS) is a terminal cell cycle arrest program, increasingly recognized as a tumor suppressor mechanism complementing apoptosis in response to standard chemotherapy regimens. In particular cells with blocked apoptotic pathways rely on senescence as the only remaining failsafe mechanism to keep the neoplastic growth in check. However, little is known about biological properties, long-term fate of senescent tumor cells and their impact on the microenvironment. We used global gene expression profiling by microarrays to gain insight in the molecular programme underlying the treatment-induced senescence in Emu-myc transgenic B-cell lymphomas (apoptosis protected by Bcl2 overexpression), which robustly enter senescence in response to DNA-damaging anticancer agents such as Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc transgenic mice were used. In this model the the c-Myc oncogene is constitutively expressed in the cells of B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas, resembling Burkitt lymphoma in humans. In order to bring up the senescence as the main failsafe mechanism, primary lymphoma cells are protected from apoptosis by retroviral over-expression of a strong antiapoptotic protein Bcl2. These cells (Myc;Bcl2) massively undergo senescence upon DNA-damaging treatment. Adriamycin (ADR) is a cytostatic drug, used as a standard part of several lymphoma treatment regimens. In this study, transcriptional profiles of matched pairs of untreated vs. 5 days ADR treated Myc;Bcl2 lymphomas were analysed.

2011-11-21 | E-GEOD-31099 | biostudies-arrayexpress

Homeobox protein NKX2-3 modulates lymphocyte dynamics and promotes B-cell lymphomagenesis

Project description:Molecular cloning of a t(10;14)(q24;q32) from a B-cell lymphoma showed a recurrent breakpoint in homeobox NKX2-3 gene, which was highly expressed in comparison to non-expressing mature B lymphocytes. Epigenetically-mediated NKX2-3 over-expression was selectively found in patients with splenic marginal-zone lymphoma, MALT lymphoma and extranodal diffuse large-cell lymphoma. In young mice, restricted expression of NKX2-3 to lymphocytes activated multiple integrins (LFA-1, VLA-4, MAC-1), adhesion molecules (ICAM-1, MadCAM-1, L-selectin) and the chemokine receptor CXCR4 that enhanced their homing and migration to splenic tissues, whereby they were retained, progressively accumulating to form non-clonal tumors. At 18 months, B cells acquired genomic rearrangements and generated clonal B-cell lymphomas mirroring the spectrum of human NKX2-3-expressing tumors. Mouse and human lymphomas displaying NKX2-3 expression shared histopahological, genomic and molecular features, including canonical NF-KB activation. NF-KB inhibition reduced tumorigenecity of NKX2-3-positive lymphomas. Our study reveals that oncogenic NKX2-3 promotes B-cell lymphomagenesis by disturbing lymphocyte dynamics. Comparisson of global gene expression profiling between Emu-NKX2-3 transgenes mice and wild type mice.

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).

2024-06-01 | GSE183695 | GEO

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

Project description:The type II nuclear receptors (NRs) function as heterodimeric transcription factors with the retinoid X receptor (RXR) to regulate diverse biological processes in response to endogenous ligands and therapeutic drugs. DNA-binding specificity has been proposed as a primary mechanism for NR gene regulatory specificity. We use protein-binding microarrays (PBMs) to comprehensively analyze the DNA binding of 12 NR:RXRα heterodimers. We find more promiscuous NR-DNA binding than has been reported, challenging the view that NR binding specificity is defined by half-site spacing. We show that NRs bind DNA using two distinct modes, explaining widespread NR binding to half-sites in vivo. Finally, we show that the current models of NR specificity better reflect binding-site activity rather than binding-site affinity. Our rich dataset and revised NR binding models provide a framework for understanding NR regulatory specificity and will facilitate more accurate analyses of genomic datasets.

2019-01-12 | GSE124910 | GEO

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).

2007-11-06 | E-GEOD-6980 | biostudies-arrayexpress

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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