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Dysplasia; Human papillomas virus; Pap smear
The human papilloma virus (HPV) is the main cause and risk factor of cervical cancer. HPV has been detected in virtually all invasive cervical cancers. About 1 in 4 U.S. females ages 14 - 59 are infected with HPV. The prevalence of HPV is highest (45%) in women ages 20 - 24.
HPV causes genital warts. However, both men and women can be infected with the HPV virus and not have any visible warts on the genitalia. This is because this virus lives in the cells.
How HPV Is Transmitted. HPV is spread primarily by having sex with an infected partner. Most sexually active young women become infected with this virus, but only 10% remain infected for more than 5 years. In most cases, HPV goes away on its own. The risk for cervical cancer in infected women appears to be highest in those with persistent long-term HPV infection. Generally, those infected for longer than 5 years have a higher risk (about 50% above normal).
How HPV Contributes to Cervical Cancer. Researchers believe that most cervical cancers develop when various aggressive genetic HPV strains activate certain oncogenes (cancer-causing genes). These oncogenes interfere with certain protective proteins, which normally limit cell growth. Once they are blocked, cell growth can run rampant, leading to tumor development and cancer.
HPV Genetic Types. More than 30 genetic variants of human papillomaviruses can be passed through sexual contact form one person to another. The severity, however, varies widely according to genetic type. (Women initially infected by one type of HPV are still at risk for infection from other types.)
Certain genetic types are low risk. They may cause cervical intraepithelial neoplasia I (6 and 11), or genital warts (condylomata) on a woman's vagina or vulva (40, 42, 43, 44, 54, 61, 70, 72, and 81). These viral types rarely lead to cancer.
Of the high-risk types, HPV types 16 and 18 have long been known to be particularly dangerous. These two genetic types and six others (31, 33, 35, 45, 52, and 58) account for 95% of HPV-related cervical cancers. Other high-risk types are 39, 51, 56, 59, 68, 73, and 82. All are associated with moderate cervical intraepithelial neoplasia II and cervical intraepithelial neoplasia III. Types 26, 53, and 66 are also considered high risk.
High-risk types of HPV have also been associated with an increased risk for other cancers, including other genital cancers, and lung and possibly oropharyngeal (throat, tongue, soft palate) cancers. The high-risk viruses generally produce flat and nearly invisible growths, compared to the usually harmless warts caused by low-risk HPV viruses.
Committee on Infectious Diseases. Prevention of human papillomavirus infection: provisional recommendations for immunization of girls and women with quadrivalent human papillomavirus vaccine. Pediatrics. 2007 Sep;120(3):666-8.
Dunne EF, Unger ER, Sternberg M, McQuillan G, Swan DC, Patel SS, et al. Prevalence of HPV infection among females in the United States. JAMA. 2007 Feb 28;297(8):813-9.
FUTURE II Study Group. Quadrivalent vaccine against human papillomavirus to prevent high-grade cervical lesions. N Engl J Med. 2007 May 10;356(19):1915-27.
Garland SM, Hernandez-Avila M, Wheeler CM, Perez G, Harper DM, Leodolter S, et al. Quadrivalent vaccine against human papillomavirus to prevent anogenital diseases. N Engl J Med. 2007 May 10;356(19):1928-43.
Hildesheim A, Herrero R, Wacholder S, Rodriguez AC, Solomon D, Bratti MC, et al. Effect of human papillomavirus 16/18 L1 viruslike particle vaccine among young women with preexisting infection: a randomized trial. JAMA. 2007 Aug 15;298(7):743-53.
Huang CM. Human papillomavirus and vaccination. Mayo Clin Proc. 2008;83(6):701-6.
Hunter MI, Monk BJ and Tewari KS. Cervical neoplasia in pregnancy. Part 1: screening and management of preinvasive disease. Am J Obstet Gynecol. 2008;199(1):3-9.
Hunter MI, Tewari K and Monk BJ. Cervical neoplasia in pregnancy. Part 2: current treatment of invasive disease. Am J Obstet Gynecol. 2008;199(1):10-8.
Long HJ 3rd, Laack NN and Gostout BS. Prevention, diagnosis, and treatment of cervical cancer. Mayo Clin Proc. 2007;82(12):1566-74.
Markowitz LE, Dunne EF, Saraiya M, Lawson HW, Chesson H, Unger ER; Centers for Disease Control and Prevention (CDC); Advisory Committee on Immunization Practices (ACIP). Quadrivalent human papillomavirus vaccine: Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2007 Mar 23;56(RR-2):1-24.
Mayrand MH, Duarte-Franco E, Rodrigues I, Walter SD, Hanley J, Ferenczy A, et al. Human papillomavirus DNA versus Papanicolaou screening tests for cervical cancer. N Engl J Med. 2007;357(16): 1579-88.
Naucler P, Ryd W, Tornberg S, Strand A, Wadell G, Elfgren K, et al. Human papillomavirus and Papanicolaou tests to screen for cervical cancer. N Engl J Med. 2007;357(16):1589-97.
Ronco G, Cuzick J, Pierotti P, Cariaggi MP, Dalla Palma P, Naldoni C, et al. Accuracy of liquid based versus conventional cytology: overall results of new technologies for cervical cancer screening: randomised controlled trial. BMJ. 2007 Jul 7;335(7609):28. Epub 2007 May 21.
Saslow D, Castle PE, Cox JT, Davey DD, Einstein MH, Ferris DG, et al. American Cancer Society Guideline for human papillomavirus (HPV) vaccine use to prevent cervical cancer and its precursors. CA Cancer J Clin. 2007 Jan-Feb;57(1):7-28.
Wright TC Jr., Massad LS, Dunton CJ, Spitzer M, Wilkinson EJ and Solomon D. 2006 consensus guidelines for the management of women with abnormal cervical cancer screening tests. Am J Obstet Gynecol. 2007;197(4): 346-55.
Wright TC Jr., Massad LS, Dunton CJ, Spitzer M, Wilkinson EJ and Solomon D. 2006 consensus guidelines for the management of women with cervical intraepithelial neoplasia or adenocarcinoma in situ. Am J Obstet Gynecol. 2007;197(4): 340-5.
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