Folate Deficiency, FHIT Hypermethylation and HPV 16 Infection Promote Cervical Cancerization

Cervical cancer is one of the most common cancers in women globally and is responsible for the large percentage of women’s death in developing countries. Epidemiological and laboratory data have shown that persistent infection with oncogenic human papillomavirus (HPV), particularly HPV-16 and HPV-18, is the main risk factor, but not solely responsible for the development of cervical cancer. Other cofactors including genetic and epigenetic factors, may facilitate the progression of cervical cancer as well. Previous studies have reported that DNA methylation of genes is a frequent epigenetic factor in cervical cancer (Piyathilake et al., 2010). Aberrant DNA methylation in the CpG islands at the promoter region is an important epigenetic mechanism underlying the inactivation of tumor suppressor genes (Abouzeid et al., 2011).