Analysis of bcl-2 expression in normal, inflamed, dysplastic nasopharyngeal epithelia, and nasopharyngeal carcinoma: Association with p53 expression

To further characterize bcl-2 expression in nasopharyngeal carcinoma (NPC), the authors analyzed bcl-2 expression immunohistochemically in biopsy specimens from 101 cases of NPC, of which 65 had the component of normal nasopharyngeal epithelium (NPE), 24 with dysplastic lesions adjacent to carcinoma, and 14 with both primary and metastatic lesions. An additional 25 nasopharyngeal biopsies of NPE from patients with chronic inflammation of nasopharynx were also included. The percentage of detectable bcl-2 expression shown in NPC (80%) and adjacent dysplastic lesions (71%) was significantly higher than in adjacent NPE (37%) and NPE from patients with chronic inflammation of the nasopharynx (30%) (P <.05). In both normal and inflamed NPE, the detectable bcl-2 expression was restricted to the basal cells; however, in dysplastic lesions, the bcl-2 staining distribution was increased with the dysplastic cell layers, and in entire layers of epithelium in severe dysplasia or carcinoma in situ. In addition, the staining intensity of bcl-2 in carcinomas and adjacent dysplastic lesions was generally stronger than that of adjacent NPE. These observations suggest that the expression of bcl- 2 in dysplasia and carcinoma is enhanced relative to that of adjacent NPE. Enhanced bcl-2 expression to prevent apoptosis seems to occur from die early stages and may play an important role in the carcinogenesis of NPC. Furthermore, up to 77% of NPC with die coexpression of bcl-2 and p53 was observed and suggested that the association of bcl-2 and p53 expression seems to occur from the early stages of the development of NPC. The overexpression of p53 protein in NPC suggests that the mutation of p53 gene or altered function of wild-type p53 protein may contribute to the pathogenesis. It is conceivable that the presence of both enhanced bcl-2 expression and altered p53 functions may play a crucial synergistic effect in die carcinogenesis of NPC.