Abstract: Nowadays, almost all of the genes in the human genome have been sequenced. The challenge now is to understand the molecular mechanisms that allow these genes to be selectively expressed. Although all genes are transcribed in an organism at some stage of its life cycle, a more restricted number are required for the differentiation of a specialized cell type. Remarkably, it is essential to select not only the correct genes to turn on, but also those that need to be inactivated. Failure to repress genes appropriately has been connected to many human diseases, including neurodevelopmental disorders and cancer. Notable among the mechanisms that stably inactivate genes in a heritable manner is DNA methylation and the associated assembly of repressive hetrochromatine. DNA methylation in mammalian cells occurs at the 5-position of cytosine within the CpG dinucleotide..Although CpG islands account for only about 1% of the genome and for 15% of the total genomic CpG sites, these regions contain over 50% of the unmethylated CpG dinucleotides. There are about 45,000 CpG islands, most of which reside within or near the promoters or first exons of genes and are unmethylated in normal cells,with the exception of CpG islands on the inactive X chromosome in general. Oral cancer continues to be a significant health problem that more people die from oral cancer than melanoma, cervical, and ovarian cancer combined. Early diagnosis significantly improves tumor control and survival. The five-year survival for patients with stage I or II oral cancer is 70 percent to 80 percent. In contrast, patients with stage III or IV oral cancer have a survival rate of only 40 percent to 50 percent. Dental health care professionals are commonly required to evaluate patients with potentially malignant oral lesions. Methylation is one of the earliest events in oral carcinogenesis, preceding changes in protein expression level. These advantages make promoter hypermethylation a very attractive diagnostic marker for the early detection of oral cancer. The hypothesis of this project is that the presence of oral cancer leads to changes in promoter hyper methylation. Therefore, is to quantitatively analyze promoter hypermethylation of five genes (APC, E-cadherin, MGMT, p15(INK4B), and p16(INK4A)) in patients and healthy groups. Current studies with tissue DNA reveal these genes are most often inactivated by promoter hypermethylation, allowing for the progression of oral cancer.

Brief Biography of the Speaker:
Upon completion of my doctorate in Biotechnology at the University of Panjab, Chandigarh, India in 2008, I joined as faculty at Department of Biology, University of Sistan and Baluchistan ,Zahedan -Iran. So, My study will provide help in finding any diagnostic biomarkers in deferent population which can use as targets that finally lead to the development of molecular technique for early diagnosis of cancer patients and susceptible individual. Currently, I have focused on effect of Methylation on oral cavity cancer. Till now I had published many international papers in this regard.