Melanoma Inhibitory Activity and Melanoma Inhibitory Activity 2 as Novel Immunohistochemical Markers of Oral Epithelial Dysplasia

Journal of Clinical Medicine

Hatsuhiko Maeda¹  Takehiro Hattori¹  Katsutoshi Kubo¹  Toshikatsu Suzumura¹  Ryoko Kawai¹  Yoshihiko Sugita¹  Waka Yoshida¹ 

[1] Department of Oral Pathology/Forensic Odontology, School of Dentistry, Aichi Gakuin University, Nagoya 464-8650, Japan;

关键词: oral epithelial dysplasia;    oral potentially malignant disorders;    oral squamous cell carcinoma;    melanoma inhibitory activity;    diagnostic marker;   

DOI  :  10.3390/jcm10163661

来源: DOAJ

【 摘 要 】

Oral potentially malignant disorders are associated with the development of oral squamous cell carcinoma (OSCC). Most OSCCs are diagnosed via histopathology as oral epithelial dysplasia (OED), but the histologic diagnostic criteria remain non-uniform. Accordingly, the establishment of a diagnostic marker to assist in diagnosis could contribute towards cancer prevention. Melanoma inhibitory activity (MIA) and MIA2 are involved in tumor growth, invasion, and lymph node metastasis in various malignancies. The purpose of this study was to clarify the usefulness of MIA and MIA2 as diagnostic markers of oral mucosal lesions. The expression of MIA and MIA2 was analyzed immunohistochemically in 100 specimens (10 specimens with normal oral mucosa (NOM) and 30 specimens each with low-grade epithelial dysplasia (LED), high-grade epithelial dysplasia (HED), and OSCC). Immunohistochemical results were evaluated based on the Allred scoring system. Cytoplasmic expression of MIA and MIA2 increased in the order of LED, HED, and OSCC. All NOM specimens were negative for cytoplasmic expression. Significant differences were observed between the groups (NOM vs. HED, p < 0.05, NOM vs. OSCC, p < 0.001). These results demonstrate that MIA and MIA2 are expressed in the oral mucosa within early neoplastic lesions and suggest that MIA and MIA2 are useful novel immunohistochemical markers for discriminating between normal tissue and OED.

【 授权许可】

Unknown