ArticleDiagnostic pathology2014
Amplification of Mdmx and overexpression of MDM2 contribute to mammary carcinogenesis by substituting for p53 mutations.
Article in Diagnostic pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 64 citations in OpenAlex.
- Role of MDM2 309T>G (rs2279744) and I/D (rs3730485) polymorphisms and haplotypes in risk of papillary thyroid carcinoma, tumor stage, tumor size, and early onset of tumor: A case control study.Journal of cellular physiology · 2019Trial
- The influence of the secretome from human amniotic mesenchymal stem cells on p53 and MDM2 expression in MDA-MB-231 breast cancer cell line.Discover oncology · 2026Article
- When the Clock Is Ticking: The Role of Mitotic Duration in Cell Fate Determination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Review
- Computational identification of potential natural terpenoid inhibitors of MDM2 for breast cancer therapy: molecular docking, molecular dynamics simulation, and ADMET analysis.Frontiers in chemistry · 2025Article
- Targeting MDM2-p53 interaction for breast cancer therapy.Oncology research · 2025Review
- Unraveling the Guardian: p53's Multifaceted Role in the DNA Damage Response and Tumor Treatment Strategies.International journal of molecular sciences · 2024Review
- Cucurbitacin B Inhibits the Proliferation of WPMY-1 Cells and HPRF Cells via the p53/MDM2 Axis.International journal of molecular sciences · 2024Article
- Death-associated protein kinase 1 phosphorylates MDM2 and inhibits its protein stability and function.Archives of pharmacal research · 2023Article
- p53 Dysregulation in Breast Cancer: Insights on Mutations in theInternational journal of molecular sciences · 2023Article
- Review
- CCDC106 promotes the proliferation and invasion of ovarian cancer cells by suppressing p21 transcription through a p53-independent pathway.Bioengineered · 2022Article
- Correlation between p53 and Mdm2 expression with histopathological parameters in cattle squamous cell carcinomas.Veterinary world · 2022Article
- Hesperidin Inhibits the p53-MDMXInteraction-Induced Apoptosis of Non-Small-Cell Lung Cancer and Enhances the Antitumor Effect of Carboplatin.Journal of oncology · 2022Article
- Article
- First in class dual MDM2/MDMX inhibitor ALRN-6924 enhances antitumor efficacy of chemotherapy in TP53 wild-type hormone receptor-positive breast cancer models.Breast cancer research : BCR · 2021Article
- Associations ofJournal of clinical medicine · 2021Article
- MDM2 as a Rational Target for Intervention in CDK4/6 Inhibitor Resistant, Hormone Receptor Positive Breast Cancer.Frontiers in oncology · 2021Review
- MDM2 inhibition in combination with endocrine therapy and CDK4/6 inhibition for the treatment of ER-positive breast cancer.Breast cancer research : BCR · 2020Article
- Biology and pathogenesis of human osteosarcoma.Oncology letters · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe p53 tumor suppressor gene is mutated or deleted in nearly half of human cancers. The murine double minute 2 (Mdm2) and Mdmx represent two important cellular regulators of p53. The aim of this study was to evaluate the abnormalities of p53, Mdmx and Mdm2 genes in archived breast cancers.
methodsWe assessed the genetic instability at p53, Mdmx and Mdm2 using high resolution multi-color fluorescent in situ hybridization (FISH) protocol and detected the expression status of the tumor protein p53 (TP53), MDMx and MDM2 by immunohistochemistry in 115 archived samples of infiltrating ductal breast carcinomas with foci of ductal carcinoma in situ (DCIS) components.
resultsThe presence of p53 allelic loss and/or TP53 overexpression was observed in 38% out of all patients, and was significantly more often in larger, high grade, ER negative and high ki67 tumors. Mdmx amplification with low-level increase of gene copy number is at high frequency while Mdm2 amplification is rare in primary breast cancer. Mdmx amplification was seen in more invasive carcinomas than preinvasive lesions. MDMx and MDM2 overexpression were detected in 65% and 38% of all cases respectively. Moreover it was showed that most tumors contained either p53 dysfunction or Mdm2 alteration, but not both. This distribution was significant (P < 0.05). Inverse correlation between Mdmx amplification/overexpression and p53 disfunction was also observed (P < 0.05).
conclusionsOur results suggest the involvement of Mdm2 and Mdmx in p53-independent breast carcinogenesis and Mdmx may contribute to the regulation of p53 independently of Mdm2. VIRTUAL SLIDES: The virtual slides for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1450529994118798.
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