Abstract

Cervical cancer is the second most common cause of female cancer mortality worldwide, accounting for approximately 274,000 deaths annually (Parikh, Brennan, & Boffetta, 2003; World Health Organization, 2002). Of the estimated 500,000 new cases of cervical cancer diagnosed each year, 80% of these occur in developing countries, with the highest rates occurring in Africa, Asia, and Central and South America (de Sanjose et al., 2010; Ferlay et al., 2010; Lipson et al., 1995; Parikh et al., 2003; World Health Organization, 2002, 2011). Human papillomavirus (HPV) has been detected in 99% of cervical cancer cases, and infection with HPV is a prerequisite to the development of invasive cervical cancer (de Sanjose et al., 2010; Dunne et al., 2007; Ferlay et al., 2010; Lipson et al., 1995; Parikh et al., 2003; World Health Organization, 2002, 2011). Seventy percent of cervical cancers are due to high-risk (HR) HPV types 16 and 18, and although there is some geographic variation in the prevalence of HPV, global data suggests that the eight most common high-risk oncogenic HPV genotypes (16, 18, 21, 33, 35, 45, and 52) contribute to over 90% of the cervical cancer in all world regions [de Sanjose, 2010; Dunne, 2007; World Health Organization, 2011].

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