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Cancer of the cervix is the third most common gynecologic malignancy in the United States. In 2015, a total of 12,900 new cases of cervical cancer and 4,100 deaths are estimated (1). The incidence of this disease has decreased steadily over the past several decades. However, cervical cancer remains one of the most common cancers in women worldwide with approximately 527,600 new cases diagnosed each year and 265,700 related deaths (2).
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Squamous cell carcinoma (SCC) of the cervix may occur at any age from the second decade of life onward. The mean age at diagnosis is approximately 51.4 years, with the number of cases evenly divided between patients at 30 to 39 and 60 to 69 years of age (3). Adenocarcinoma makes up to 15% to 25% of all invasive cervical cancers.
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Etiology and Risk Factors
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Risk factors for cervical cancer are listed in Table 33-1.
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To understand the current methods for cervical screening, a basic understanding of the nature of cervical abnormalities is essential. Human papillomavirus (HPV) is the critical factor for the development of preinvasive and invasive cervical lesions. More than 14 million incident cases are reported annually, the majority of which occur in persons age 15 to 24 years (4,5,6). HPV is a small, nonenveloped, double-stranded DNA virus predominantly transmitted through sexual intercourse. The most consistent risk factors for acquiring HPV are number of sexual partners, age of first sexual intercourse, and a partner infected with HPV.
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More than 40 genotypes of HPV infect the epithelial lining of the anogenital tract and other mucosal areas of the body (7). These subtypes are further classified into high-risk HPV (HR-HPV) and low-risk HPV (LR-HPV) depending on their oncogenic potential for cervical cancer and its precursors. Low-risk HPV genotypes include HPV-6 and -11 and typically cause benign anogenital warts, although they may occasionally be associated with neoplastic cervical changes (8). Invasive lesions, on the other hand, are much more commonly caused by HR-HPV including, in order of frequency, types 16, 18, 31, 45, 52, and 33 (9). Although the majority of premalignant and invasive disease can be directly attributed to types 16 or 18, HPV DNA from any genotype is detectable in greater than 99% of all cervical cancer specimens (8).