# Mutation of PTEN: Loss and Likelihood of Being a Non-responder to Trastuzumab in a Sample of Iraqi Her2+ Breast Cancer Patients

**Authors:** Alyaa H Hammadi, Shatha H Ali

PMC · DOI: 10.7759/cureus.54765 · Cureus · 2024-02-23

## TL;DR

This study finds that PTEN gene loss is more common in Her2+ breast cancer patients who do not respond to trastuzumab treatment.

## Contribution

The study identifies PTEN loss as a potential predictor of non-response to trastuzumab in Her2+ breast cancer patients.

## Key findings

- PTEN loss was observed in 26.67% of non-responders compared to 3.33% of responders.
- PTEN loss showed a statistically significant difference between responder and non-responder groups.
- PTEN loss was not associated with changes in CK-MB, TnT, or TnI biomarkers during treatment.

## Abstract

Introduction: PTEN controls upstream PI3K relatives, such as AKT. PTEN gene mutations have been documented to affect outcomes in main or distant malignancies, including breast cancer (BC). PTEN gene deletions are common in a variety of human cancers. A key factor in the response to this kind of therapy is genetic diversity. The purpose of this research is to determine whether a PTEN loss mutation influences a patient's propensity to not respond to trastuzumab (TRS) in cases of Her2+ BC.

Methods: Diwaniya Teaching Hospital's oncology ward provided 60 patients with Her2+ BC who had been on TRS for at least 12 months for this study. Patients were split in half using the RECIST criteria for evaluating responses to therapy in solid tumors: responders and non-responders. A PTEN polyclonal primary antibody was used for the detection of PTEN in breast tissue in the current study.

Results: This research employs a rating system based on eight specimens (26.67%) among non-responsive women who demonstrated PTEN loss compared with one specimen (3.33%) among responsive women. Statistically, PTEN loss varied significantly between the responsive and non-responsive groups. Loss of PTEN was also not linked to shifts in creatine kinase-myocardial band (CK-MB), troponin T (TnT), or any other biomarker, or troponin I (Tn1) at baseline or after 12 months of TRS therapy.

These results give us important information about how PTEN deletion mutations might work as a predictor for TRS response in women with Her2+ BC.

## Linked entities

- **Genes:** PTEN (phosphatase and tensin homolog) [NCBI Gene 5728]
- **Proteins:** AKT1 (AKT serine/threonine kinase 1)
- **Diseases:** breast cancer (MONDO:0004989)

## Full-text entities

- **Genes:** ERBB2 (erb-b2 receptor tyrosine kinase 2) [NCBI Gene 2064] {aka CD340, HER-2, HER-2/neu, HER2, MLN 19, MLN-19}, TNNT1 (troponin T1, slow skeletal type) [NCBI Gene 7138] {aka ANM, NEM5, STNT, TNT, TNTS}, PTEN (phosphatase and tensin homolog) [NCBI Gene 5728] {aka 10q23del, BZS, CWS1, DEC, GLM2, MHAM}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}
- **Diseases:** cancers (MESH:D009369), BC (MESH:D001943)
- **Chemicals:** TRS (MESH:D000068878)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC10961105/full.md

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Source: https://tomesphere.com/paper/PMC10961105