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Cervical Cancer Prevention (PDQ®)

Description of Evidence

Incidence and Mortality

An estimated 12,900 new cervical cancers and 4,100 cervical cancer deaths will occur in the United States in 2015.[1] An additional 1,250,000 women will be diagnosed with precancers annually by cytology using the Papanicolaou (Pap) smear. A continuum of pathologic changes may be diagnosed, ranging from atypical squamous cells of undetermined significance to low-grade squamous intraepithelial lesions (LSIL) to high-grade squamous intraepithelial lesions (HSIL) to invasive cancer. The precancerous conditions LSIL and HSIL are also referred to as cervical intraepithelial neoplasia (CIN) 1, 2, and 3. Lesions can regress, persist, or progress to an invasive malignancy, with LSIL (CIN 1) more likely to regress spontaneously and HSIL (CIN 2/CIN 3) more likely to persist or progress. The average time for progression of CIN 3 to invasive cancer is estimated to be 10 to 15 years.[2]

The incidence of cervical cancer has decreased dramatically with the advent and widespread adoption of screening via gynecological examinations and Pap smears (refer to the PDQ summary on Cervical Cancer Screening for more information). Regular screening, however, is associated with large numbers of diagnostic procedures to evaluate abnormal tests, and the treatment of low-grade lesions may adversely affect subsequent fertility and pregnancy. Prevention of cancer may be more efficient, with fewer adverse consequences.

Nearly all cases of cervical cancer are associated with human papillomavirus (HPV) infection, which is transmitted during sexual activity. Therefore, cervical cancer is seen more frequently in women with sexual activity at an early age and with multiple partners. Barrier contraception and/or spermicidal gels may offer some protection.[3] (Refer to the Human Papillomavirus section of this summary for more information.)

Cigarette smoking or exposure to environmental smoke is also associated with increased risk among HPV-infected women,[4] suggesting that components of tobacco are promoters of abnormal growth of viral-infected cells.

References

  1. American Cancer Society: Cancer Facts and Figures 2015. Atlanta, Ga: American Cancer Society, 2015. Available online. Last accessed January 7, 2015.
  2. Holowaty P, Miller AB, Rohan T, et al.: Natural history of dysplasia of the uterine cervix. J Natl Cancer Inst 91 (3): 252-8, 1999. [PUBMED Abstract]
  3. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: Human papillomaviruses. IARC Monogr Eval Carcinog Risks Hum 100 (Pt B), 255-313, 2012. Available online. Last accessed February 10, 2015.
  4. Ho GY, Kadish AS, Burk RD, et al.: HPV 16 and cigarette smoking as risk factors for high-grade cervical intra-epithelial neoplasia. Int J Cancer 78 (3): 281-5, 1998. [PUBMED Abstract]
  • Updated: February 17, 2015