Loss of BCL-2 in the progression of oral cancer is not attributable to mutations
- 1Department of Odontology-Oral Pathology and Forensic Odontology, Haukeland University Hospital, N5021 Bergen, Norway
- 2Department of Pathology, The Gade Institute, University of Bergen, Haukeland University Hospital
- Correspondence to: Dr L L Loro Department of Odontology-Oral Pathology and Forensic Odontology, The Gade Institute, Haukeland University Hospital, N5021 Bergen, Norway; lado.lorogades.uib.no
- Accepted 21 March 2005
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.
- BH, BCL-2 homology
- ISH, in situ hybridisation
- OED, oral epithelial dysplasia
- OSCC, oral squamous cell carcinoma
- PCR, polymerase chain reaction
- SNP, single nucleotide polymorphism
