IADR Abstract Archives
DAPK1 and DCC Hypermeyjylation in Oral Lichen Planus
Objectives: The aim of this study was to investigate the expression of hypermethylated DAPK1 and DCC genes and DAPK/DCC proteins in OLP, comparing them with OL and OSCC in order to evaluate their potential use as predictive biomarkers.
Methods: DAPK1 and DCC hypermethylation was evaluated in tissue samples from the Department of Oral Medicine/Pathology, School of Dentistry, Aristotle University of Thessaloniki, Greece, including 21 OLPs (Reticular and Erosive forms), 62 OLs (Hyperkeratosis Mild, Moderated/Severe dysplasia), 39 OSCCs (well-differentiated, moderately-differentiated and poorly-differentiated) and 12 normal oral tissues. DNA-hypermethylation was evaluated using bisulfate conversion and Methylation specific PCR-MSP techniques whereas DAPK1/DCC molecules’ expression was detected via paraffin immunohistochemical analysis (IHC).
Results: DAPK1 and DCC hypermethylation was found in 30% and 55% of OLP respectively. All OLP expressed DAPK1 whereas 78% of them expressed DCC molecule.
Significant difference in DAPK1-hypemethylation was found between ΟLP forms (higher in erosive ) (p=0,007) and between ΟLP and OSCC (higher in OSCC) (p<0,001). The DAPK1 IHC expression was significantly higher in OLP than compared to OSCC and OL with moderated-severe dysplasia (p<0,001, p=0,002 respectively) . Regarding DCC-hypermethylation, statistically significant difference was found between OLP and OSCC (p<0,001) (higher in OSCC).
Conclusions: DAPK1 and DCC genes are epigenetically inactivated by hypermethylation in most cases of OSCC but not in OL or OLP suggesting a non-premalignant background. Whether this OLP-hypermethylation in specific cases is related with precancerous or cancerous progression needs further investigation. DAPK1 protein is mainly expressed in ΟLP and less in OSCC or moderated-severe dysplasia OL supporting its tumor suppressive activity in OLP.
Methods: DAPK1 and DCC hypermethylation was evaluated in tissue samples from the Department of Oral Medicine/Pathology, School of Dentistry, Aristotle University of Thessaloniki, Greece, including 21 OLPs (Reticular and Erosive forms), 62 OLs (Hyperkeratosis Mild, Moderated/Severe dysplasia), 39 OSCCs (well-differentiated, moderately-differentiated and poorly-differentiated) and 12 normal oral tissues. DNA-hypermethylation was evaluated using bisulfate conversion and Methylation specific PCR-MSP techniques whereas DAPK1/DCC molecules’ expression was detected via paraffin immunohistochemical analysis (IHC).
Results: DAPK1 and DCC hypermethylation was found in 30% and 55% of OLP respectively. All OLP expressed DAPK1 whereas 78% of them expressed DCC molecule.
Significant difference in DAPK1-hypemethylation was found between ΟLP forms (higher in erosive ) (p=0,007) and between ΟLP and OSCC (higher in OSCC) (p<0,001). The DAPK1 IHC expression was significantly higher in OLP than compared to OSCC and OL with moderated-severe dysplasia (p<0,001, p=0,002 respectively) . Regarding DCC-hypermethylation, statistically significant difference was found between OLP and OSCC (p<0,001) (higher in OSCC).
Conclusions: DAPK1 and DCC genes are epigenetically inactivated by hypermethylation in most cases of OSCC but not in OL or OLP suggesting a non-premalignant background. Whether this OLP-hypermethylation in specific cases is related with precancerous or cancerous progression needs further investigation. DAPK1 protein is mainly expressed in ΟLP and less in OSCC or moderated-severe dysplasia OL supporting its tumor suppressive activity in OLP.