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Updated: Mar 23, 2026
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Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
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p53 expression and relationship with MDM2 amplification in breast carcinomas
Nur Buyukpinarbasili1, Zuhal Gucin1, Yeliz Emine Ersoy2
1Department of Pathology, Bezmialem Vakif University, 34093 Fatih, Istanbul, Turkey.
Annals of Diagnostic Pathology
|April 5, 2016
Summary
p53 and MDM2 interactions are crucial in breast cancer. While MDM2 amplification is infrequent, its functional loss impacts p53 tumor suppression, particularly in HER-2 and triple-negative breast carcinoma subtypes.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Breast carcinoma is a genetic disease driven by multiple genetic events.
- p53 mutations are common in human cancers, and MDM2 regulates p53 stability.
- MDM2 inactivation can lead to loss of p53 tumor suppressor function.
Purpose of the Study:
- To analyze p53 and MDM2 status in human sporadic breast carcinoma.
- To investigate the interaction between p53 and MDM2 in different breast cancer subtypes.
- To evaluate the role of MDM2 amplification and p53 expression in breast carcinogenesis.
Main Methods:
- Molecular classification of 92 breast carcinoma cases into Luminal A, Luminal B, HER-2 positive, and triple-negative subtypes.
- Statistical comparison of p53 and MDM2 status, histologic type, and prognostic parameters across subtypes.
- Analysis of p53 expression and MDM2 amplification frequency.
Main Results:
- p53 expression was lower in Luminal breast carcinomas compared to HER-2 and triple-negative subtypes.
- MDM2 gene amplification occurred in 5.4% of the cases.
- MDM2 amplification did not show a significant role in breast carcinogenesis, suggesting other inactivation mechanisms.
Conclusions:
- p53 and MDM2 interactions are critical in breast cancer development.
- MDM2 gene amplification is not a primary driver in breast carcinogenesis.
- Further investigation into alternative MDM2 inactivation mechanisms is warranted.
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