Predicting transition from oral pre-malignancy to malignancy via Bcl-2 immuno-expression: Evidence and lacunae

通过Bcl-2免疫表达预测口腔癌前病变向恶性肿瘤的转变:证据与不足

阅读:1

Abstract

Bcl-2 (B cell Lymphoma -2) family comprises of both anti-apoptotic and pro-apoptotic proteins whose altered expression or change in ratio inhibits apoptosis, and promotes tumor progression. The aim of this study is to assess the usefulness of Bcl-2 in distinguishing dysplastic or malignant epithelium from non-dysplastic or normal epithelium to aid in prediction of malignant transformation potential. MATERIAL AND METHOD: Study group comprised of 30 cases of clinically diagnosed leukoplakia (OPMD), 15 cases of Oral Squamous Cell Carcinoma (OSCC) and 5 normal tissue samples. The labeling index of Bcl-2 was analyzed in immunohistochemically stained sections. Different statistical tools were used to analyze the data and to compare Bcl-2 expression qualitatively and quantitatively among all the groups. RESULTS: An increasing trend of Bcl-2 immunoexpression was observed from normal epithelium to non-dysplastic and from non-dysplastic to dysplastic lesions. In OSCC, the peripheral cells in the differentiating epithelial islands (within the connective tissue) showed Bcl-2 immuno-reactivity, which gradually decreased towards the center. In contrast, intense and diffuse Bcl-2 immuno-reactivity was seen in poorly differentiated carcinoma. But the overall Bcl-2 positivity was less in OSCC as compared to dysplastic lesions. CONCLUSION: Increased expression of Bcl-2 oncoprotein in sequentially progressing epithelial dysplasia and down-regulation in differentiating carcinoma (well and moderately differentiating OSCC) unveils the clinical relevance of Bcl-2 in early stages of OSCC tumorigenesis. The heterogenous expression of Bcl-2 in carcinoma with different grades of differentiation renders them unable to be used as an independent tool for predicting transition from oral pre-malignancy to malignancy.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。