MTHFR C677T Polymorphism and Cervical Cancer Risk: a Meta-Analysis

Cervical cancer is the third most commonly diagnosed cancer and the fourth leading cause of cancer death in the females worldwide, accounting for 9% (529,800 cases) of the total new cancer cases and 8% (275,100 deaths) of the total cancer deaths among females in 2008 (Jemal et al., 2011). More than 85% of these cases and deaths occur in developing countries (Jemal et al., 2011, Li et al., 2011). Epidemiological studies have confirmed that oncogenic subtypes of the human papilloma virus (HPV) are a crucial etiological factor of cervical tumorigenesis (Walboomers et al., 1999; Munoz et al., 2003). However, this virus is cleared by the immune system in the majority of HPV infected women and only stays in the few individuals, with the oncogenic subtypes resulting in cervical cancer (Munger et al., 2004; Mun et al., 2011). Thus, this information suggests a remarkable interaction between the virus and the host’s genetic factors, which may increase the host’s susceptibility to cervical cancer (Magnusson et al., 1999; Baseman and Koutsky, 2005). The 5, 10-methylenetetrahydrofolate reductase gene (MTHFR) maps to chromosome 1p36.3, and MTHFR plays a central role in folate metabolism, together with other enzymes by irreversibly catalyzing the conversion of 5, 10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, the primary circulating form of folate and a cosubstrate for homocysteine methylation to methionine (Goyette et al., 1994; Goyette et al., 1998). Many rare mutations of