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Most women with HPV infection, however, never develop cervical cancer thus, this infection is necessary but not sufficient for the development of cancer.Īlthough cervical cancer mortality increases with age, the prevalence of CIN is highest among women in their 20s and 30s. Nearly all women with invasive cervical cancer have evidence of HPV infection. Sexually inactive women rarely develop cervical cancer, while sexual activity at an early age with multiple sexual partners is a strong risk factor. Human papillomavirus (HPV) is an oncogenic virus and the etiologic agent of cervical cancer and related premalignant disease. Because many of these preinvasive lesions (especially LSILs) would have never progressed to invasive cancer, screening also runs the risk of leading to treatment for women who do not need to be treated. This long natural history provides the opportunity for screening to effectively detect this process during the preinvasive phase, thus allowing early treatment and cure. The rate at which invasive cancer develops from CIN is usually slow, measured in years and perhaps decades.
NET SENSITIVITY OF SEQUENTIAL TESTING PLUS
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 (LSILs), LSILs (consisting of cytologic atypia and CIN 1), and high-grade squamous intraepithelial lesions (HSILs), primarily CIN 2–3 plus carcinoma in situ. Not all of these lesions progress to invasive cancer many mild and moderate lesions regress. CIN is histologically graded into mild dysplasia (CIN 1), moderate dysplasia (CIN 2), or severe dysplasia (CIN 3). Invasive squamous carcinoma of the cervix results from the progression of preinvasive precursor lesions called cervical intraepithelial neoplasia (CIN), or dysplasia. When corrected for the prevalence of hysterectomy, the mortality rate for Black women is nearly twice the mortality rate for White women. This improvement has been attributed largely to screening with the Papanicolaou (Pap) test. From 2010 to 2019, the pace of decline in the death rate decreased by 0.8% per year. Incidence rates have stabilized in the most recent decade. These rates have been improving steadily. In the United States in 2022, it is estimated that 14,100 cases of invasive cervical cancer will be diagnosed and that 4,280 women will die of the disease. Natural History, Incidence, and Mortality Ronco G, Dillner J, Elfström KM, et al.: Efficacy of HPV-based screening for prevention of invasive cervical cancer: follow-up of four European randomised controlled trials.Chen HC, Schiffman M, Lin CY, et al.: Persistence of type-specific human papillomavirus infection and increased long-term risk of cervical cancer.Szarewski A: Cervical screening by visual inspection with acetic acid.Sankaranarayanan R, Nene BM, Shastri SS, et al.: HPV screening for cervical cancer in rural India.Wright TC, Stoler MH, Behrens CM, et al.: Primary cervical cancer screening with human papillomavirus: end of study results from the ATHENA study using HPV as the first-line screening test.Kyrgiou M, Athanasiou A, Paraskevaidi M, et al.: Adverse obstetric outcomes after local treatment for cervical preinvasive and early invasive disease according to cone depth: systematic review and meta-analysis.Preventive Services Task Force recommendation statement. Preventive Services Task Force: Screening for cervical cancer: U.S. Sawaya GF, McConnell KJ, Kulasingam SL, et al.: Risk of cervical cancer associated with extending the interval between cervical-cancer screenings.Sasieni P, Castanon A, Cuzick J: Effectiveness of cervical screening with age: population based case-control study of prospectively recorded data.Study Design: Evidence obtained from a single cohort study.