Nearly two decades ago, experts discovered a relationship between infection with HPV (human papillomavirus) and cervical cancer. Since then, these experts have learned much more about how HPV can lead to cervical cancer.
Here, what every woman and girl should know about this link.
In the United States in 2013, it is estimated that 12,340 cases of invasive cervical cancer will be diagnosed and that 4,030 women will die of the disease. These rates had been improving steadily. However, from 2005 to 2009, rates were stable in women younger than 50 years and decreased by 3.0% per year in women aged 50 years and older. From 2005 to 2009, mortality rates were stable among women of all ages. This improvement has been attributed largely to screening with the Papanicolaou (Pap) test.
Invasive squamous carcinoma of the cervix results from the progression of preinvasive precursor lesions called cervical intraepithelial neoplasia (CIN), or dysplasia. CIN is histologically graded into mild dysplasia (CIN 1), moderate dysplasia (CIN 2), or severe dysplasia (CIN 3). Not all of these lesions progress to invasive cancer; many mild and moderate lesions regress. A further categorization, the Bethesda system, is based on cytologic findings: atypical squamous cells of undetermined significance (ASCUS) or cannot rule out low-grade squamous intraepithelial lesions (LSIL), LSIL (consisting of cytologic atypia and CIN 1), and high-grade squamous intraepithelial lesions (HSIL), primarily CIN 2–3 plus carcinoma in situ.
The rate at which invasive cancer develops from CIN is usually slow, measured in years and perhaps decades. This long natural history provides the opportunity for screening to effectively detect this process during the preinvasive phase, thus allowing early treatment and cure. Because many of these preinvasive lesions (especially LSIL) would have never progressed to invasive cancer,[4,5,6] screening also runs the risk of leading to treatment for women who do not need to be treated.
Human papillomavirus (HPV) is an oncogenic virus and the etiologic agent of cervical cancer and related premalignant disease. HPV is transmitted by sexual contact. Sexually inactive women rarely develop cervical cancer, while sexual activity at an early age with multiple sexual partners is a strong risk factor. Nearly all women with invasive cervical cancer have evidence of HPV infection.[8,9,10,11] Most women with HPV infection, however, never develop cervical cancer; thus this infection is necessary but not sufficient for development of cancer.
Although cervical cancer mortality increases with age, the prevalence of CIN is highest among women in their 20s and 30s. Mortality is rare among women younger than 30 years; HSIL is rare among women older than 65 years who have been previously screened. About 70% of ASCUS and CIN 1 lesions regress within 6 years, while about 6% of CIN 1 lesions progress to CIN 3 or worse. In about 10% to 20% of women with CIN 3 lesions, the lesions progress to invasive cancer.[3,6,14]