Release Date: 21 November 2011

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

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  • Maja Milanovic
    Maja Milanovic
    Email: maja.milanovic@charite.de
    Role: submitter
    Affiliation: Charite University Medicine, Berlin
    1
  • Clemens Schmitt
    Clemens Schmitt
  • Michael Hummel
    Michael Hummel
  • Dido Lenze
    Dido Lenze
  • Jan Dörr
    Jan Dörr
  • Yong Yu
    Yong Yu
  • 1 Charite University Medicine, Berlin
    Address: Hematology and Oncology, Charite University Medicine, Berlin, Augustenburgerplatz 1, Berlin, Germany
AccessionE-GEOD-31099
Study typetranscription profiling by array
OrganismMus musculus
DescriptionTreatment 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.
Publication Jing H, Kase J, Dörr JR, Milanovic M, Lenze D, Grau M, Beuster G, Ji S, Reimann M, Lenz P, Hummel M, Dörken B, Lenz G, Scheidereit C, Schmitt CA, Lee S. Opposing roles of NF-κB in anti-cancer treatment outcome unveiled by cross-species investigations. doi 10.1101/gad.17620611 PMID 21979374 DOI 10.1101/gad.17620611
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.
Protocols show table
Samples
Sample count24
Experimental FactorsSENESCENCE INDUCTION, TREATMENT
Experimental Factors
Source Characteristics
Assays and Data
TechnologyArray assay
Assay by MoleculeRNA assay
Raw Data
Processed Data
MAGE-TAB Files
Array Designs 1 link
MIAME Score
Platforms-
Processed*
Raw*
Variables*
Protocols-