“…Cervical cancer development is the result of complex interactions between the host and environmental factors, undergoing stepwise progression from low-grade to high-grade dysplasia to invasive carcinoma. In this pathway, activation or inactivation of various cancer-related genes is involved [3,17,31,39]. Recent studies have demonstrated the promoter hypermethylation of several genes, such as DAPK, p16 INK4A , O6-methylguanine-DNA methyltransferase (MGMT), APC, HIC-1, E-cadherin, RARß, FHIT, GSTP and hMLH1, associated with cervical carcinogenesis [13,24,43,45,48].…”