Global expression profiling of Emu-myc lymphomas
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ABSTRACT:
PROVIDER: PRJNA167838 | ENA |
REPOSITORIES: ENA
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Project description:Therapy-induced senescence (TIS) is a DNA damage-triggered irreversible cell-cycle block that terminates further expansion of (pre-)malignant lesions. Utilizing the Eµ-myc transgenic mouse lymphoma model (apoptosis protected by retroviral Bcl2-overexpression), we sought to elucidate the 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 into the molecular program 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).
2020-12-31 | GSE38285 | GEO
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
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
Project description:Genome-wide binding targets of PRDM15 were identified in Emu-Myc Lymphomas
2019-07-04 | GSE116905 | GEO
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. 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.
2020-03-19 | GSE134751 | GEO
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
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
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).
2020-04-15 | GSE134753 | GEO
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).
2011-11-21 | GSE31099 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-12-31 | GSE38429 | GEO