Analysis of the Promoter Hypermethylation of Chosen Tumor Suppressor Genes in Laryngeal Cancer

Abstract

Background: DNA hypermethylation is one of the epigenetic mechanisms leading to transcriptional inactivation of genes and shows tissue and tumor-type specificity. Methods:We evaluated DNA deletions/duplications as well as hypermethylation status of chosen tumor suppressors in 57 laryngeal squamous cell carcinomas using MS-MLPA. Results:We observed a significantly higher frequency of gene methylation and deletions in cancer cells compared to normal laryngeal cells. In tumor cells, hypermethylation is also often observed at ESR1 and CDH13, TIMP3, RARB, while CDKN2B hypermethylation appears to be increased in both normal and tumor cells. Deletions suggest the presence of genetic instability in LSCC and in tumors are associated with low values of tumor size and stage. The risk of metastases increased with at least 3 deletions in the laryngeal tumor, in particular with deletion at the FHIT locus, also with at least 3 hypermethylated sites in normal laryngeal cells. Conclusion:The results of our study confirm involvement of both epigenetic and genetic events in laryngeal cancer development.