Cervical cancer is cancer of the cervix, the lower end of a woman's uterus. It is preceded by a precancerous condition called CIN (cervical intraepithelial neoplasia) or cervical dysplasia which may or may not develop into cancer.
Cervical cancer is the sixth most common cancer in women in the United States and the most common cancer in women in many economically underdeveloped countries. Only breast cancer causes more cancer-related deaths in women worldwide.
The rate of cervical cancer has been decreasing steadily over the past several decades in the United States, due in large part to widespread routine Pap smear screening. A Pap smear is used to detect the early growth of precancerous CIN cells in the cervix and is the single most important step a woman can take to prevent cervical cancer. In many developing countries where preventative health measures are not routine, the incidence and mortality from cervical cancer continue to rise.
Various studies have predicted that, if left untreated, anything between 15% and 70% of CIN cases will eventually develop into invasive cervical cancer.
HIV-infected women are more likely to acquire human papillomavirus (HPV), including the high-risk subtypes 16 and 18 that can lead to cervical dysplasia and cervical cancer. HIV-infected women also have increased persistence of HPV.
Women who are negative for HPV have little or no risk of developing cervical cancer.
It has been shown that genes play an important part in this disease: a woman has a higher risk of cervical cancer if her sister or mother had it.
A primary risk factor for cervical cancer is a weakened immune system. Since infection with HIV, for example, damages the immune system, being HIV-positive makes women more susceptible to HPV infection and cervical cancer.
African-American women are more at risk of cervical cancer than are Caucasians.
In a five year follow-up study, women whose blood had shown signs of infection with any type of chlamydia were about 21⁄2 times more likely to develop cervical cancer, compared with those who had not had signs of infection. Women with one particular subtype of chlamydia in their blood (serotype G) were 6 times more likely to develop cervical cancer, and several other subtypes were linked to risks 3 to 4 times that of uninfected women.
Increased risk is associated with early onset of sexual activity.
Increased risk is associated with multiple sexual partners.
Early childbearing increases the risk.
Cigarette smoking accounts for approximately 30% of cervical cancers deaths in the USA, with women smokers having a two-fold increase in the incidence of this disease over never-smokers. Cessation appears to have an immediate effect, with former smokers having no increased risk of developing cervical cancer.
A 9-year prospective study of over 6,000 women found a dose-response relationship between smoking cigarettes and the risk of cervical cancer. Those who smoked 15 or more cigarettes per day were 80% more likely to develop cancer or precancerous lesions than nonsmokers. Those who smoked for 10 or more years were 80% more likely to develop cancer. Starting smoking younger than age 16 produced twice the risk of nonsmokers for developing cervical pathology. Smoking is one co-factor that makes HPV-infected cells more likely to turn cancerous.
HPV confers a very high risk of developing cervical cancer; all cases of cervical cancer are positive for HPV. Cervical cancer is the first major solid tumor cancer to be identified as being caused by a virus.
A study of women found that the 75% who ate the least amount of tomatoes had between 3.5 and 4.7 times the risk for cervical intraepithelial neoplasia – pre-cancerous changes of the cervix. [Int J Cancer 1991;48: pp.34-8] Other researchers have also reported evidence suggesting that high dietary lycopene may be linked to protection from cervical dysplasia. [Nutr Cancer 1998;31: pp.31-40]
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