Cervical Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI]

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Cervical Cancer Prevention (PDQ®): Prevention - Health Professional Information [NCI]

This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.

Cervical Cancer Prevention


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

Avoidance of Human Papillomavirus Infection

Based on solid evidence, the following measures are effective to avoid human papillomavirus (HPV) infection, and thus cervical cancer:

Abstinence from sexual activity

Magnitude of Effect: Abstinence prevents HPV infection.

Study Design: Evidence obtained from cohort and case-control studies.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.

Barrier protection and/or spermicidal gel during sexual intercourse

Magnitude of Effect: Total use of barrier protection decreases cancer incidence, relative risk of 0.4 (95% confidence interval [CI], 0.2–0.9).

Study Design: Evidence obtained from cohort and case-control studies.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.

Based on fair evidence, vaccination against HPV-16/HPV-18 is effective to avoid HPV infection, and thus cervical cancer.

Magnitude of Effects: Vaccination against HPV-16 and HPV-18 reduces incident and persistent infections with efficacy of 91.6% (95% CI, 64.5–98.0) and 100% (95% CI, 45–100), respectively. Efficacy beyond 6 to 8 years is not known.

Study Design: Evidence obtained from randomized controlled trials.
Internal Validity: Good.
Consistency: Not applicable.
External Validity: Good.

Screening via Gynecologic Examinations and Cytologic Screening

Based on solid evidence, screening via regular gynecologic examinations and cytologic test (Papanicolaou smear) with treatment of precancerous abnormalities decreases the incidence and mortality of cervical cancer. Screening is not beneficial in detecting invasive cancer in women younger than 25 years because of the low prevalence of invasive disease, and the harms outweigh the benefits. Screening is not beneficial in women older than 60 years if they have had a history of recent negative tests.

Magnitude of Effect: Estimates from population studies suggest that screening may decrease cancer incidence and mortality by more than 80%.

Study Design: Evidence obtained from cohort or case-control studies.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.

Cigarette Smoke

Based on solid evidence, cigarette smoking, both active and passive, increases the risk of cervical cancer.

Magnitude of Effect: Among HPV-infected women, current and former smokers have approximately two to three times the incidence of high-grade cervical intraepithelial neoplasia or invasive cancer. Passive smoking is also associated with increased risk, but to a lesser extent.

Study Design: Evidence obtained from cohort or case-control studies.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.

Reproductive Behavior

High parity

Based on solid evidence, high parity is associated with increased risk of cervical cancer.

Magnitude of Effect: Among HPV-infected women, those who have had seven or more full-term pregnancies have approximately four times the risk of squamous cell cancer compared with nulliparous women, and two to three times the risk of women who have had one or two full-term pregnancies.[1]

Study Design: Evidence obtained from cohort or case-control studies.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.

Long-term use of oral contraceptives

Based on solid evidence, long-term use of oral contraceptives is associated with increased risk of cervical cancer.

Magnitude of Effect: Among HPV-infected women, those who used oral contraceptives for 5 to 9 years have approximately three times the incidence of invasive cancer, and those who used them for 10 years or longer have approximately four times the risk.[2]

Study Design: Evidence obtained from cohort or case-control studies.
Internal Validity: Good.
Consistency: Good.
External Validity: Good.


1. Muñoz N, Franceschi S, Bosetti C, et al.: Role of parity and human papillomavirus in cervical cancer: the IARC multicentric case-control study. Lancet 359 (9312): 1093-101, 2002.
2. Moreno V, Bosch FX, Muñoz N, et al.: Effect of oral contraceptives on risk of cervical cancer in women with human papillomavirus infection: the IARC multicentric case-control study. Lancet 359 (9312): 1085-92, 2002.

Description of Evidence

Incidence and Mortality

An estimated 12,170 new cervical cancers and 4,220 cervical cancer deaths will occur in the United States in 2012.[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,[3,4] 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 (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,[5] suggesting that components of tobacco are promoters of abnormal growth of viral-infected cells.


1. American Cancer Society.: Cancer Facts and Figures 2012. Atlanta, Ga: American Cancer Society, 2012. Available online. Last accessed June 14, 2012.
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.
3. zur Hausen H, de Villiers EM: Human papillomaviruses. Annu Rev Microbiol 48: 427-47, 1994.
4. 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.
5. 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.

Evidence of Benefit

Human Papillomavirus

Epidemiologic studies to evaluate risk factors for the development of squamous intraepithelial lesions (SIL) and cervical malignancy demonstrate conclusively a sexual mode of transmission of a carcinogen.[1] It is now widely accepted that human papillomavirus (HPV) is the primary etiologic infectious agent.[2,3,4] Other sexually transmitted factors, including herpes simplex virus 2 and Chlamydia trachomatis, may play a cocausative role.[1] The finding of HPV viral DNA integrated in most cellular genomes of invasive cervical carcinomas supports epidemiologic data linking this agent to cervical cancer;[5] however, direct causation has not been demonstrated. More than 80 distinct types of HPV have been identified, approximately 30 of which infect the human genital tract. HPV types 16 and 18 are most often associated with invasive disease. Characterization of carcinogenic risk associated with HPV types is an important step in the process of developing a combination HPV vaccine for the prevention of cervical neoplasia. In a population-based study of HPV infection and cervical neoplasia in Costa Rica, 80% of high-grade squamous intraepithelial lesions (HSIL) and invasive lesions were associated with HPV infection by one or more of 13 cancer-associated types.[6] In this study, the risk of about half of HSIL and invasive cervical cancer was attributable to HPV-16. HPV-18 was associated with 15% of invasive disease but only 5% of HSIL, suggesting that HPV-18 may have a role in more aggressive cases of cervical malignancy.

Barrier methods of contraception are associated with a reduced incidence of SIL presumptively secondary to protection from sexually transmitted disease.[7,8] The effectiveness of condom use for the prevention of HPV infections has been evaluated in a prospective study of women aged 18 to 22 years who were virgins.[9] The number of vulvovaginal HPV infections was reduced with consistent condom use, and HPV infection rate was 37.8 infections per 100 patient-years among women whose partners used condoms 100% of the time in the 8 months before testing, compared with 89.3 infections per 100 patient-years among women whose partners used condoms less than 5% of the time (P trend = .005). No cervical SIL were detected among women reporting 100% condom use by their partner.[9]

Given the etiologic role of HPV in the pathogenesis of cervical neoplasia, vaccines to immunize against HPV infection would offer a primary prevention strategy for cervical cancer. A quadrivalent (HPV 6, 11, 16, and 18) vaccine using a late protein L1 construct to induce antibody-mediated immunity was approved for use by the U.S. Food and Drug Administration in 2006; a bivalent (HPV 16, 18) vaccine was approved in 2009.

Vaccine to prevent HPV infection

Persistent infection with oncogenic types of HPV such as HPV-16 and HPV-18 is associated with the development of cervical cancer.[10] A vaccine to prevent HPV infection with oncogenic-type viruses has the potential to reduce the incidence of cervical cancer. A vaccine against HPV-16 using empty-viral capsids called virus-like particles (VLP) was developed and tested for efficacy in preventing persistent infection with HPV-16.

A multicenter, double-blind, placebo-controlled trial enrolled 2,391 women aged 16 to 23 years and randomly assigned them to receive either 40 µg of HPV-16 L1 VLP vaccine or placebo on day 1, at 2 months, and at 6 months. Papanicolaou (Pap) tests and genital samples for HPV-16 DNA were obtained on day 1, at 7 months, and every 6 months for 48 months. Colposcopy and cervical biopsies were obtained when clinically indicated at study exit. Serum HPV-16 antibody titers were obtained at study entry, at 7 months, and then every 6 months. A total of 1,505 women (755 receiving vaccine and 750 receiving placebo) completed all three vaccinations and had follow-up after month 7. After immunization, HPV titers peaked at month 7, declined through month 18, and then stabilized in months 30 through 48. There were no cases of cervical intraepithelial neoplasia (CIN) in the vaccine-treated women, but there were 12 cases in the placebo group (six CIN 2 and six CIN 3). HPV-16 infection that persisted for at least 4 months was seen in seven vaccine-treated women versus 111 placebo-treated women.[11]

An international, double-blind, placebo-controlled trial of a bivalent HPV-16/HPV-18 VLP vaccine was performed in 1,113 women aged 15 to 25 years with normal cervical cytology who were seronegative for HPV-16, HPV-18, and 12 other oncogenic HPV types at enrollment. Women received either vaccine or placebo at 0, 1, and 6 months and were assessed by cervical cytology and self-obtained cervicovaginal samples for at least 18 months. A masked treatment allocation follow-up study was performed for an additional 3 years, for a combined analysis of up to 6.4 years of follow-up. The 12-month persistent infection rate of HPV-16 or HPV-18 in an "according-to-protocol" cohort (i.e., women who received all three doses of vaccine or placebo on the correct schedule) was 0 of 401 women in the vaccine arm versus 20 of 372 women in the placebo arm, with a vaccine efficacy of 100% (95% confidence interval [CI], 81.8–100). Diagnoses of CIN 2 or higher in a "total vaccinated" cohort (i.e., women who received at least one dose of vaccine or placebo) were 0 of 481 women in the vaccine arm versus 9 of 470 women in the placebo arm, with a vaccine efficacy of 100% (95% CI, 51.3–100). Adverse events were similar in vaccinated and placebo-treated women. It is important to note that neither analysis was intention-to-treat (ITT), making it difficult to know what the true vaccine efficacy for either virological or cytohistological endpoints would be in the routine clinical setting. Furthermore, cytohistological outcomes were reported only as composite endpoints (CIN 2+), making it impossible to distinguish the vaccine's efficacy against invasive cervical cancer alone and potentially inflating the observed efficacy by including lesions with a relatively high probability (approximately 50% for CIN 2 [12]) of spontaneous regression.[13]

A quadrivalent vaccine (HPV types 6, 11, 16, and 18) was evaluated in a multinational, double-blind, randomized controlled trial of 17,622 women aged 15 to 26 years (FUTURE I and II).[14] Women received either the HPV vaccine or placebo at 0, 2, and 6 months; participants were assessed by clinical exam, Pap test, and HPV DNA testing for 4 or more years. Two analyses were reported. One group was considered to be HPV naive: negative to 14 HPV types. The second group was an ITT analysis, which approximates a sexually active population. The composite endpoint for cervical disease included the incidence of HPV-16/18-related, CIN 2, CIN 3, adenocarcinoma in situ, or invasive carcinoma. Outcomes were reported as follows:

Vaccine Efficacy of the Quadrivalent HPV Vaccine

PopulationPoint Estimate and 95% CI
CIN = cervical intraepithelial neoplasia; HPV = human papillomavirus; ITT = intention-to-treat.
HPV naive population for HPV-CIN 3100% (90.5%–100%) for lesions associated with HPV 6, 11,16, or 18
ITT CIN 345.3% (29.8%–57.6%) for lesions associated with HPV 6, 11, 16, or 18

This study also demonstrated decreased rates of abnormal Pap tests and subsequential diagnostic procedures. No cases of invasive cervical cancer were identified during the trial.

As largely expected based upon their mechanism of action, L1/2 HPV vaccines do not appear to impact pre-existing infections. The FUTURE II trial demonstrated a markedly lower vaccine efficacy rate in the total randomized study population, which included individuals positive for HPV at baseline, versus the "per-protocol" population (44% for lesions associated with HPV 16 or 18 and 17% for lesions associated with any HPV type vs. 98%, see table above).[14] Additionally, an intermediate analysis of a randomized controlled trial primarily evaluating the efficacy of the HPV-16/18 vaccine in preventing infection found no effect on viral clearance rates in women aged 18 to 25 years who were positive at the time of study enrollment.[15]

The type-specific vaccines, if successful in preventing invasive cancer, will offer protection for only a subset of cases, the proportion of which will vary worldwide.[16] Using data from a multicenter case-control study conducted in 25 countries, it was estimated that a vaccine containing the seven most common HPV types could prevent 87% of cervical cancers worldwide. A vaccine with HPV-16 and HPV-18 types, the two most common strains, would prevent 71% of cervical cancers worldwide.[16]

Anal HPV infection

Anal cancer occurs rarely: the international age-adjusted annual incidence is about 1.5 cases per 100,000 women.[17] However, rates have been increasing in Europe and the United States over the past few decades. As with cervical cancer, HPV-16 and HPV-18 are associated with a majority of anal cancer cases. To estimate the efficacy of the bivalent vaccine against anal HPV infections in women, investigators examined a subset of women participating in a randomized controlled trial principally designed to assess vaccine efficacy against persistent cervical HPV-16/18 infections and associated precancerous lesions. In the original trial,[15] 6,352 women aged 18 to 25 years received three doses of the bivalent vaccine or a control hepatitis A vaccine and were followed for 4 years after first administration. Women that attended the 4-year study visit, consented to provide anal specimens, and completed a survey regarding anal sexual behaviors (n=4,210) were included in this secondary analysis.[18] The efficacy of the vaccine against prevalent HPV-16/18 anal infections was 62% (95% CI, 47.1–73.1) for an ITT cohort. Limitations of this study include an inability to assess the baseline anal HPV infection rate in the population or to use HPV persistence as the endpoint of interest; given a high rate of spontaneous resolution of HPV infection, the endpoint of HPV prevalence will overestimate the efficacy of the vaccine. Additionally, there was a high attrition rate: the subgroup represented 56% of the original trial participants, of which 27% were lost due to noncompliance with anal sampling. The study provides no information about the efficacy of the vaccine against precancerous anal lesions or anal cancer.

Cigarette Smoking

Cigarette smoking by women is associated with an increased risk for squamous cell carcinoma.[1,19,20] This risk increases with longer duration and intensity of smoking and may be present with exposure to environmental tobacco smoke, being as high as four times that of women who are nonsmokers and are not exposed to environmental smoking.[1] Case-control studies of women infected with HPV have examined the effect of various types and levels of tobacco exposure and found similar results.[20,21]

Reproductive Behavior

High parity has long been recognized as a risk factor for cervical cancer, but the relation of parity to HPV infection was uncertain. A meta-analysis of 25 epidemiologic studies, including 16,563 women with cervical cancer and 33,542 women without cervical cancer, showed that the number of full-term pregnancies was associated with increased risk, regardless of age at first pregnancy. This finding was also true if analyses were limited to patients with high-risk HPV infections (relative risk = 4.99 [3.49–7.13] for seven or more pregnancies versus no pregnancies; linear trend test x2 = 30.69; P < .001).[22]

Long-term use of oral contraceptives has also been known to be associated with cervical cancer, but its relation to HPV infection was also uncertain. A pooled analysis of HPV-positive women from the studies described above was undertaken. Compared with women who have never used oral contraceptives, those who have used them for fewer than 5 years did not have an increased risk of cervical cancer (odds ratio [OR] = 0.73; 95% CI, 0.52–1.03). The OR for women who used oral contraceptives for 5 to 9 years was 2.82 (1.46–5.42), and for 10 or more years, the OR was 4.03 (2.09–8.02).[23] A meta-analysis of 24 epidemiological studies confirmed the increased risk associated with oral contraceptives, which is proportionate to the duration of use. Risk decreases after cessation and returns to normal risk levels in 10 years.[24]

Dietary Factors

Multiple case-control studies show an association between intake of some micronutrients and lower risk of cervical cancer, but results are conflicting and difficult to control for other risk factors. Two randomized trials of oral folate as a chemopreventive agent have shown no protective effect.


1. Brinton LA: Epidemiology of cervical cancer--overview. IARC Sci Publ (119): 3-23, 1992.
2. 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.
3. 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.
4. 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.
5. Reeves WC, Rawls WE, Brinton LA: Epidemiology of genital papillomaviruses and cervical cancer. Rev Infect Dis 11 (3): 426-39, 1989 May-Jun.
6. Herrero R, Hildesheim A, Bratti C, et al.: Population-based study of human papillomavirus infection and cervical neoplasia in rural Costa Rica. J Natl Cancer Inst 92 (6): 464-74, 2000.
7. 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.
8. 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.
9. Winer RL, Hughes JP, Feng Q, et al.: Condom use and the risk of genital human papillomavirus infection in young women. N Engl J Med 354 (25): 2645-54, 2006.
10. Wallin KL, Wiklund F, Angström T, et al.: Type-specific persistence of human papillomavirus DNA before the development of invasive cervical cancer. N Engl J Med 341 (22): 1633-8, 1999.
11. Mao C, Koutsky LA, Ault KA, et al.: Efficacy of human papillomavirus-16 vaccine to prevent cervical intraepithelial neoplasia: a randomized controlled trial. Obstet Gynecol 107 (1): 18-27, 2006.
12. Castle PE, Schiffman M, Wheeler CM, et al.: Evidence for frequent regression of cervical intraepithelial neoplasia-grade 2. Obstet Gynecol 113 (1): 18-25, 2009.
13. Romanowski B, de Borba PC, Naud PS, et al.: Sustained efficacy and immunogenicity of the human papillomavirus (HPV)-16/18 AS04-adjuvanted vaccine: analysis of a randomised placebo-controlled trial up to 6.4 years. Lancet 374 (9706): 1975-85, 2009.
14. FUTURE II Study Group.: Quadrivalent vaccine against human papillomavirus to prevent high-grade cervical lesions. N Engl J Med 356 (19): 1915-27, 2007.
15. Hildesheim A, Herrero R, Wacholder S, et al.: Effect of human papillomavirus 16/18 L1 viruslike particle vaccine among young women with preexisting infection: a randomized trial. JAMA 298 (7): 743-53, 2007.
16. Muñoz N, Bosch FX, Castellsagué X, et al.: Against which human papillomavirus types shall we vaccinate and screen? The international perspective. Int J Cancer 111 (2): 278-85, 2004.
17. Stewart BW, Kleihues P, eds.: World Cancer Report 2003. Lyon, France: International Agency for Research on Cancer, 2003. Also available online. Last accessed December 13, 2011.
18. Kreimer AR, González P, Katki HA, et al.: Efficacy of a bivalent HPV 16/18 vaccine against anal HPV 16/18 infection among young women: a nested analysis within the Costa Rica Vaccine Trial. Lancet Oncol 12 (9): 862-70, 2011.
19. 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.
20. 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.
21. 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.
22. International Collaboration of Epidemiological Studies of Cervical Cancer.: Cervical carcinoma and reproductive factors: collaborative reanalysis of individual data on 16,563 women with cervical carcinoma and 33,542 women without cervical carcinoma from 25 epidemiological studies. Int J Cancer 119 (5): 1108-24, 2006.
23. Moreno V, Bosch FX, Muñoz N, et al.: Effect of oral contraceptives on risk of cervical cancer in women with human papillomavirus infection: the IARC multicentric case-control study. Lancet 359 (9312): 1085-92, 2002.
24. Appleby P, Beral V, Berrington de González A, et al.: Cervical cancer and hormonal contraceptives: collaborative reanalysis of individual data for 16,573 women with cervical cancer and 35,509 women without cervical cancer from 24 epidemiological studies. Lancet 370 (9599): 1609-21, 2007.

Changes to This Summary (01 / 13 / 2012)

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

Description of Evidence

Updated statistics with estimated new cases and deaths for 2012 (cited American Cancer Society as reference 1).

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About This PDQ Summary

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about cervical cancer prevention. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

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Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

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National Cancer Institute: PDQ® Cervical Cancer Prevention. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/prevention/cervical/HealthProfessional. Accessed <MM/DD/YYYY>.

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