L L Loro1, A C Johannessen, O K Vintermyr. 1. Department of Odontology-Oral Pathology and Forensic Odontology, Haukeland University Hospital, N5021 Bergen, Norway.
Abstract
BACKGROUND: BCL-2 and BAX are important in the regulation of apoptosis. There have been reports of loss of BCL-2 in basal cells of oral epithelial dysplasia (OED) and in oral squamous cell carcinoma (OSCC), and suppression of BAX in poorly differentiated OSCC. AIM: To investigate whether loss of BCL-2 in OED and OSCC, and of BAX in poorly differentiated OSCC could be attributed to BCL-2 and BAX mutations. METHODS: Immunohistochemistry and in situ hybridisation were used to confirm BCL-2 and BAX expression. DNA was extracted from archival samples of OED (n = 22) and OSCC (n = 28). The connective tissue part from each section was collected separately and used as the normal reference. RESULTS: No mutations were detected in BCL-2 or BAX that could explain their aberrant expression at the mRNA and protein levels in OED and OSCC. The reported A/G polymorphism at codon 7 of BCL-2 was detected in 18 of 50 samples and a novel C/T polymorphism at codon 100 was detected in three of 50 samples. CONCLUSIONS: No mutations were found that could explain loss of BCL-2 in oral dysplasia and carcinoma. An unreported C/T polymorphism in BCL-2 was detected. Downregulation of BCL-2 in OED and OSCC may be the result of transcriptional regulation.
BACKGROUND:BCL-2 and BAX are important in the regulation of apoptosis. There have been reports of loss of BCL-2 in basal cells of oral epithelial dysplasia (OED) and in oral squamous cell carcinoma (OSCC), and suppression of BAX in poorly differentiated OSCC. AIM: To investigate whether loss of BCL-2 in OED and OSCC, and of BAX in poorly differentiated OSCC could be attributed to BCL-2 and BAX mutations. METHODS: Immunohistochemistry and in situ hybridisation were used to confirm BCL-2 and BAX expression. DNA was extracted from archival samples of OED (n = 22) and OSCC (n = 28). The connective tissue part from each section was collected separately and used as the normal reference. RESULTS: No mutations were detected in BCL-2 or BAX that could explain their aberrant expression at the mRNA and protein levels in OED and OSCC. The reported A/G polymorphism at codon 7 of BCL-2 was detected in 18 of 50 samples and a novel C/T polymorphism at codon 100 was detected in three of 50 samples. CONCLUSIONS: No mutations were found that could explain loss of BCL-2 in oral dysplasia and carcinoma. An unreported C/T polymorphism in BCL-2 was detected. Downregulation of BCL-2 in OED and OSCC may be the result of transcriptional regulation.
Authors: S Henderson; M Rowe; C Gregory; D Croom-Carter; F Wang; R Longnecker; E Kieff; A Rickinson Journal: Cell Date: 1991-06-28 Impact factor: 41.582