ORIGINAL ARTICLE

Loss of BCL-2 in the progression of oral cancer is not attributable to mutations

L L Loro¹, A C Johannessen¹ and O K Vintermyr²

¹ Department of Odontology-Oral Pathology and Forensic Odontology, Haukeland University Hospital, N5021 Bergen, Norway
² Department of Pathology, The Gade Institute, University of Bergen, Haukeland University Hospital

Correspondence to:
Correspondence to:
Dr L L Loro
Department of Odontology-Oral Pathology and Forensic Odontology, The Gade Institute, Haukeland University Hospital, N5021 Bergen, Norway; lado.loro{at}gades.uib.no

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.

Abbreviations: 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

Keywords: oral; cancer; dysplasia; BCL-2; BAX

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