ArticleOncogene2008
Elevated Mdm2 expression induces chromosomal instability and confers a survival and growth advantage to B cells.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 91 citations in OpenAlex.
- MDM2 inhibitors in cancer immunotherapy: Current status and perspective.Genes & diseases · 2024Review
- MDM2 Inhibitors for Cancer Therapy: The Past, Present, and Future.Pharmacological reviews · 2024Review
- Long noncoding RNA,Frontiers in cell and developmental biology · 2024Article
- Machine Learning Algorithms Identify Target Genes and the Molecular Mechanism of Matrine against Diffuse Large B-cell Lymphoma.Current computer-aided drug design · 2024Article
- Targeting AKT with costunolide suppresses the growth of colorectal cancer cells and induces apoptosis in vitro and in vivo.Journal of experimental & clinical cancer research : CR · 2021Article
- Targeting Mouse Double Minute 2: Current Concepts in DNA Damage Repair and Therapeutic Approaches in Cancer.Frontiers in pharmacology · 2020Review
- Article
- Targeting of SGK1 by miR-576-3p Inhibits Lung Adenocarcinoma Migration and Invasion.Molecular cancer research : MCR · 2019Article
- Peli1 Modulates the Subcellular Localization and Activity of Mdmx.Cancer research · 2018Article
- MDMX acidic domain inhibits p53 DNA binding in vivo and regulates tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Inactivation of ribosomal protein S27-like confers radiosensitivity via the Mdm2-p53 and Mdm2-MRN-ATM axes.Cell death & disease · 2018Article
- Decoding critical long non-coding RNA in ovarian cancer epithelial-to-mesenchymal transition.Nature communications · 2017Article
- Non-Hodgkin and Hodgkin Lymphomas Select for Overexpression of BCLW.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- NRF2 Is a Major Target of ARF in p53-Independent Tumor Suppression.Molecular cell · 2017Article
- Activation of PERK-Nrf2 oncogenic signaling promotes Mdm2-mediated Rb degradation in persistently infected HCV culture.Scientific reports · 2017Article
- Mdm2 Is Required for Survival and Growth of p53-Deficient Cancer Cells.Cancer research · 2017Article
- BCL-W has a fundamental role in B cell survival and lymphomagenesis.The Journal of clinical investigation · 2017Article
- Role of Mdm2 and Mdmx in DNA repair.Journal of molecular cell biology · 2017Review
- Regulation of the Mdm2-p53 signaling axis in the DNA damage response and tumorigenesis.Translational cancer research · 2016Article
- Histone deacetylase inhibition reveals a tumor-suppressive function of MYC-regulated miRNA in breast and lung carcinoma.Cell death and differentiation · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Mdm2, a regulator of the p53 tumor suppressor, is frequently overexpressed in lymphomas, including lymphomas that have inactivated p53. However, the biological consequences of Mdm2 overexpression in lymphocytes are not fully resolved. Here, we report that increased expression of Mdm2 in B cells augmented proliferation and reduced susceptibility to p53-dependent apoptosis, which was due to inhibition of p53 and suppression of p21 expression. Notably, developing and mature B cells from Mdm2 transgenic mice had an increased frequency of chromosomal/chromatid breaks and/or aneuploidy. This Mdm2-mediated genome instability occurred at a similar frequency as that in B cells overexpressing the oncogene c-Myc, but the chromosomal instability was not further enhanced when Mdm2 and c-Myc were overexpressed together. Elevated Mdm2 expression alone increased the occurrence of B-cell transformation in vivo and cooperated with c-Myc overexpression, resulting in an acceleration of B-cell lymphomagenesis. In addition, the frequency of p53 mutations was reduced, but not eliminated, in lymphomas arising in Mdm2/Emu-myc double transgenic mice. Therefore, increased Mdm2 expression facilitated B-cell lymphomagenesis, in part, through regulation of p53 by altering B-cell proliferation and susceptibility to apoptosis, and by inducing chromosomal instability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.