# Immunohistochemical Evaluation of ALDH1 and Maspin in Oral Potentially Malignant Disorders and Oral Carcinoma

**Authors:** Bianca-Andreea Onofrei, Delia Gabriela Ciobanu Apostol, Mădălina-Gabriela Tanasă, Elena-Raluca Baciu, Cristina Popa, Ana Maria Sciuca, George Alexandru Maftei, Victor-Vlad Costan

PMC · DOI: 10.3390/biomedicines14010079 · Biomedicines · 2025-12-30

## TL;DR

This study examines ALDH1 and Maspin protein levels in oral tissues to identify their role in predicting cancer progression from pre-cancerous conditions to oral cancer.

## Contribution

The study introduces a dual-marker model combining ALDH1 and Maspin for assessing malignant transformation risk in oral potentially malignant disorders.

## Key findings

- ALDH1 expression increases significantly in pre-cancerous and cancerous oral tissues compared to normal tissues.
- Maspin expression decreases in pre-cancerous and cancerous tissues, with the most significant reduction in oral squamous cell carcinoma.
- Combined evaluation of ALDH1 and Maspin provides a more accurate assessment of dysplastic severity and cancer risk.

## Abstract

Background/Objectives: Oral potentially malignant disorders (OPMDs), including oral leukoplakia (OLK), oral lichen planus (OLP), and actinic cheilitis (AC), have varying risks of progression to oral squamous cell carcinoma (OSCC). Biomarkers such as aldehyde dehydrogenase 1 (ALDH1) and mammary serine protease inhibitor (Maspin) have shown potential for diagnostic and prognostic use in oral cancer. The present study aimed to evaluate the immunoexpression of aldehyde dehydrogenase 1, a cancer stem cell marker associated with aggressiveness, and the mammary serine protease inhibitor, a potential tumor suppressor, in OPMD and OSCC tissues. Methods: A retrospective analysis was performed on 145 biopsy specimens collected from January 2015 to January 2023, including normal epithelium, OPMDs (OLK, OLP, AC), and OSCC. ALDH1 and Maspin expression levels were evaluated using immunohistochemistry, considering both the percentage of positive cells and staining intensity. Statistical analyses were carried out using the Statistical Package for the Social Sciences (SPSS, version 29.0; IBM Corp., Chicago, IL, USA). Results: Normal oral epithelium showed no expression of ALDH1, whereas 40.6% of OPMDs and 44.4% of OSCC samples exhibited high cytoplasmic ALDH1 expression. Nuclear ALDH1 expression was elevated in 29.7% of OPMDs and 38.9% of OSCCs (p < 0.001). Nuclear Maspin expression was high in 95.2% of normal tissues, in 67.2% of OPMDs and in 55.6% of OSCCs (p < 0.001). Maspin showed strong nuclear and cytoplasmic expression in normal tissue, but its expression decreased in OPMDs and OSCCs, with statistically significant reductions in both compartments (p < 0.001). Conclusions: The results indicate that ALDH1 upregulation and Maspin downregulation are hallmark events in oral carcinogenesis. Their combined evaluation provides a powerful tool for assessing dysplastic severity and malignant transformation risk in OPMDs. Future studies on larger cohorts are needed to confirm the prognostic utility of this dual-marker model.

## Linked entities

- **Genes:** ALDH1A1 (aldehyde dehydrogenase 1 family member A1) [NCBI Gene 216], SERPINB5 (serpin family B member 5) [NCBI Gene 5268]
- **Proteins:** ALDH1A1 (aldehyde dehydrogenase 1 family member A1), SERPINB5 (serpin family B member 5)
- **Diseases:** oral leukoplakia (MONDO:0004844), oral lichen planus (MONDO:0043923), actinic cheilitis (MONDO:0043300), oral squamous cell carcinoma (MONDO:0004958)

## Full-text entities

- **Genes:** SERPINB5 (serpin family B member 5) [NCBI Gene 5268] {aka PI5, maspin}, ALDH1A1 (aldehyde dehydrogenase 1 family member A1) [NCBI Gene 216] {aka ALDC, ALDH-E1, ALDH1, ALDH11, HEL-9, HEL-S-53e}
- **Diseases:** OSCC (MESH:D000077195), OPMD (MESH:D039141), cancer (MESH:D009369), AC (MESH:C535669), OLP (MESH:D017676), Oral Carcinoma (MESH:D009062), OPMDs (MESH:C537245), OLK (MESH:D007972), oral carcinogenesis (MESH:D063646)

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12839276/full.md

## References

27 references — full list in the complete paper: https://tomesphere.com/paper/PMC12839276/full.md

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Source: https://tomesphere.com/paper/PMC12839276