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Updated: Jun 4, 2026
Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
[PTEN gene in triple-negative breast cancer]
Abstract:
The paper gives the results of studying the expression of the PTEN gene product by an immunohistochemical method, as well as deletion of the gene by fluorescence in situ hybridization in the tumor cells of 80 patients with triple-negative breast cancer (TNBC). The gene product was absent in the tumor cell nuclei in 56 products. The bulk of the remaining patients who showed a positive response had lobular carcinomas or tumors with an unidentified microscopic variant due to secondary posttherapeutic changes. Lobular carcinomas in a control group presented by patients without TNBC also contained the PTEN gene product. Therefore, all positively responding tumor cells failed to express basaloid markers and androgen receptors. The immunohistochemically detectable absence of the PTEN gene product is usually coupled with deletion at locus 10q23; however, in several cases the negative immunohistochemical reaction is associated with no deletion at the above locus, which suggests that there are mechanisms for PTEN gene dysregulation other than deletion in TNBC. The presence of the PTEN gene product in the tumor cells is associated with good prognosis in patients with TNBC.
Insights
The PTEN gene product
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapies.
- PTEN gene alterations are implicated in various cancers, but their role in TNBC requires further elucidation.
- Understanding PTEN expression and deletion is crucial for identifying potential therapeutic targets and prognostic markers in TNBC.
Purpose of the Study:
- To investigate the expression of the PTEN gene product and PTEN gene deletion in tumor cells of patients with TNBC.
- To correlate PTEN status with clinicopathological features and prognosis in TNBC.
- To explore potential mechanisms of PTEN gene dysregulation in TNBC.
Main Methods:
- Immunohistochemistry was used to assess PTEN protein expression in tumor cell nuclei.
- Fluorescence in situ hybridization (FISH) was employed to detect PTEN gene deletion at locus 10q23.
- Analysis included 80 patients with TNBC and a control group of patients without TNBC.
Main Results:
- PTEN gene product was absent in tumor cell nuclei in 56 out of 80 (70%) TNBC patients.
- Absence of PTEN product was often associated with PTEN gene deletion at 10q23, but other dysregulation mechanisms were also observed.
- Lobular carcinomas, both in TNBC and control groups, consistently expressed the PTEN gene product.
- Presence of PTEN gene product in TNBC cells correlated with a good prognosis.
Conclusions:
- Loss of PTEN gene product expression is frequent in TNBC and can occur independently of gene deletion.
- PTEN status serves as a potential prognostic biomarker in TNBC.
- Further research into PTEN dysregulation mechanisms may reveal novel therapeutic strategies for TNBC.
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