Search

Telomerase activity is associated with most malignant tumors. To evaluate the role of telomerase reactivation as a diagnostic and prognostic marker in oral carcinogenesis activity was investigated in mortal and immortal cell lines in eight oral leukoplakias (OL) and 46 oral squamous cell carcinomas (OSCC). Activity was also investigated in 13 histopathologically unaffected mucosas from distant sites or tumor-free margins of the same patients using a modified, highly sensitive, non-radioactive telomeric repeat amplification protocol (TRAP). This was correlated with histopathological stages and the clinical course of the disease. 50% of OL and 46% of OSCC showed activity. One patient with positive, high dysplastic OL developed an OSCC 11 month later. One of three specimens of adjacent tissue presented activity and a recurrence occurred after 6 months. Out of 10 tissues of distal normal mucosa, 2 demonstrated activity which could also be proved in the corresponding tumor. Detection of telomerase reactivation may be a novel method for early detection of immortalised cell clones and malignant cells in histopathologically normal oral squamous epithelium.

In many studies the detection of p53 protein by immunohistochemistry (IHC) with one antibody is assumed to be consistent with a mutation of the gene. To determine the correlation of protein detection by immunohistochemistry and gene mutation, paraffin embedded specimens of 60 oral leukoplakias (OL) and 73 oral squamous cell carcinomas (OSCC) were analysed by IHC with two different antibodies (Do7; Pab 1801), PCR-SSCP and sequencing. In 98% of OLs and 94% of OSSCs p53 protein expression was detected with at least one antibody. Only 49% of all tissue specimen were positive with both antibodies. Molecular analysis of the same specimen showed mutations of the p53 gene in 13.3% of OLs and 9, 6% of OSCCs. p53 protein expression was not detected by IHC in 3 out of 7 OSCC with p53 mutations. According to these results detection of p53 expression by IHC is not always correlated with p53 gene mutation and failure to detect p53 protein by IHC does not prove the absence of mutation of the gene in the carcinogenesis in the oral mucosa.