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Cervical Cancer (PDQ®): Prevention
Patient VersionHealth Professional VersionLast Modified: 02/20/2004




Summary of Evidence






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Summary of Evidence

Gynecologic Examinations and Pap Tests
Human Papillomavirus (HPV)
Cigarette Smoke
Dietary Factors

Note: Separate PDQ summaries on Screening for Cervical Cancer and Cervical Cancer Treatment are also available.

Gynecologic Examinations and Pap Tests

Abundant evidence suggests that regular gynecologic examinations and Pap tests for all women beginning at the onset of sexual activity, or by approximately age 18 years if not sexually active, decreases cervical cancer incidence and mortality. An upper age limit at which such screening ceases to be effective is not known.

Levels of Evidence

3ai: Evidence obtained from well-designed and conducted cohort or case-control analytic studies, preferably from more than one center or research group that have a cancer mortality endpoint.


4ai: Ecologic (descriptive) studies that have a cancer mortality endpoint.


5: Opinions of respected authorities based on clinical experience or reports of expert committees.


Human Papillomavirus (HPV)

Evidence supports a sexual mode of transmission of a carcinogen and human papillomavirus (HPV) is strongly implicated epidemiologically as the main infectious etiologic agent.[1-3]

Preliminary evidence suggests a vaccine against HPV-16 using empty-viral capsids, called “virus-like particles,” reduces the risk of acquiring transient and persistent HPV-16 infections and cervical neoplasia. The duration of protection is unknown (Level of Evidence 1b). Adverse events were similar in women receiving vaccine and placebo. None were serious, and the most common event was pain at the site of injection. Vaccines against other oncogenic types of HPV have not been reported.

Barrier methods of contraception lower the incidence of cervical neoplasia, presumptively secondary to lessened exposure to HPV.[4,5]

Levels of Evidence

1b: Evidence obtained from at least one well-designed and conducted randomized controlled trial that has a generally accepted intermediate endpoint (e.g., large adenomatous polyps for studies of colorectal cancer prevention; high-grade squamous intraepithelial lesions of the cervix for studies of cervical cancer prevention).


3ai: Evidence obtained from well-designed and conducted cohort or case-control analytic studies, preferably from more than one center or research group that have a cancer mortality endpoint.


4ai: Ecologic (descriptive) studies that have a cancer mortality endpoint.


5: Opinions of respected authorities based on clinical experience or reports of expert committees.


Cigarette Smoke

Exposure to cigarette smoke is associated with increased risk.[6-8]

Levels of Evidence

3ai: Evidence obtained from well-designed and conducted cohort or case-control analytic studies, preferably from more than one center or research group that have a cancer mortality endpoint.


4ai: Ecologic (descriptive) studies that have a cancer mortality endpoint.


5: Opinions of respected authorities based on clinical experience or reports of expert committees.


Dietary Factors

Increased intake of micronutrients and other dietary factors such as carotenoids are associated with decreased risk.

Level of Evidence

3ai: Evidence obtained from well-designed and conducted cohort or case-control analytic studies, preferably from more than one center or research group that have a cancer mortality endpoint.


References

  1. Ley C, Bauer HM, Reingold A, et al.: Determinants of genital human papillomavirus infection in young women. J Natl Cancer Inst 83 (14): 997-1003, 1991.  [PUBMED Abstract]

  2. Muñoz N, Bosch FX, de Sanjosé S, et al.: The causal link between human papillomavirus and invasive cervical cancer: a population-based case-control study in Colombia and Spain. Int J Cancer 52 (5): 743-9, 1992.  [PUBMED Abstract]

  3. Schiffman MH, Bauer HM, Hoover RN, et al.: Epidemiologic evidence showing that human papillomavirus infection causes most cervical intraepithelial neoplasia. J Natl Cancer Inst 85 (12): 958-64, 1993.  [PUBMED Abstract]

  4. Parazzini F, Negri E, La Vecchia C, et al.: Barrier methods of contraception and the risk of cervical neoplasia. Contraception 40 (5): 519-30, 1989.  [PUBMED Abstract]

  5. Hildesheim A, Brinton LA, Mallin K, et al.: Barrier and spermicidal contraceptive methods and risk of invasive cervical cancer. Epidemiology 1 (4): 266-72, 1990.  [PUBMED Abstract]

  6. Brinton LA: Epidemiology of cervical cancer--overview. IARC Sci Publ (119): 3-23, 1992.  [PUBMED Abstract]

  7. Hellberg D, Nilsson S, Haley NJ, et al.: Smoking and cervical intraepithelial neoplasia: nicotine and cotinine in serum and cervical mucus in smokers and nonsmokers. Am J Obstet Gynecol 158 (4): 910-3, 1988.  [PUBMED Abstract]

  8. Brock KE, MacLennan R, Brinton LA, et al.: Smoking and infectious agents and risk of in situ cervical cancer in Sydney, Australia. Cancer Res 49 (17): 4925-8, 1989.  [PUBMED Abstract]

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