There are several risk factors for the development of cervical cancer, both genetic and environmental. These include:

Human Papillomavirus (HPV) Infection:

HPV infection is associated with virtually all cases of cervical cancer. HPV is among the most common sexually transmitted diseases and most women clear the infection within two years without complications. Long term infection with high-risk strains of HPV can lead to the development of cervical dysplasia and cancer.⁽¹⁾

Because of the very high correlation between HPV infection and cervical cancer, the following paragraphs describe HPV in more detail.

The Human papillomaviruses are a family of sexually transmitted viruses consisting of over 100 different viral strains, 40 of which are known to infect the human genital tract and 15 of which have been associated with cervical cancer. Most infections are asymptomatic, but some strains of HPV lead to the development of genital warts.

HPV contains a small, circular, double stranded DNA genome. The virus infects epithelial cells, one of the rapidly dividing cells that form the skin and mucous membranes. The virus reproduces within the host cell and when the cell dies, as part of natural cell turnover, the new virus particles (virions) are released and can infect other cells. The DNA of low-risk types of HPV remains separate from the host DNA, while high-risk forms are able to combine with (insert into) the host DNA. Insertion into the host genome is problematic because it interrupts the transcriptional regulation of the viral genes. Without this control, the viral genome is transcribed at a much higher rate. The HPV genome contains at least two genes whoseprotein products function as oncogenes. These genes are called E6 and E7. The E6 and E7 proteins inhibit the human tumor suppressorproteins p53 and pRb, respectively. Inactivation of p53 leads to cell immortalization and inactivation of pRb leads to increased cell division. While either one of these mutations has the potential to lead to the development of cancer, the ability of HPV to inactivate both tumor suppressors further increases the efficiency of the transformation from normal to cancerous cells.⁽²⁾

Infection with low-risk HPV strains generally produces benign lesions with a minimal chance of progression to dysplasia or cancer. However, high risk HPV strains (16, 18, 31, 33 and 35) are implicated in 99% of those diagnosed with cervical cancer. It is important to note that most women infected with high-risk strains of HPV infection will not develop cancer. The risk of developing dysplasia or cancer after HPV infection is, in part, dependent on the amount of virus present during infection and the length of time it takes to clear the infection.⁽²⁾

There is no cure or treatment for HPV infection. Even without treatment, most infections are cleared by the immune system within two years. If the infection persists there is an increased chance of viral DNA integration and progression to cancer. ⁽¹⁾Women can be tested to learn if they are infected with HPV. Even though there is currently no cure for HPV infection, the knowledge can help women make responsible choices regarding their sexual practices.

More on Tumor Suppressors and Oncogenes

Family History of Cervical Cancer:
Women with a family history of cervical cancer, especially an affected mother or sister, have a two-fold risk of developing cervical cancer, suggesting an inherited susceptibility. However, there does not appear to be a correlation between a family history of other cancer types (i.e. colon cancer) and the risk of developing cervical cancer. ⁽³⁾

Age:
Very few women under the age of 20 are diagnosed with cervical cancer and more than half of those diagnosed are between the ages of 35 and 55. The risk decreases after age 55, but 20% of cases occur in women over 60 years old. The pattern seen is due to two conflicting factors, 1) changes in sexual behaviors and 2) the tendency of genetic mutations to accumulate over time. ⁽⁴⁾

Watch the full interview with Dr. Ira Horowitz.

Sexual and Reproductive History:
Epidemiological studies have shown an increased risk for invasive cervical cancer attributable to sexual and reproductive behavior. Increased numbers of sexual partners and lower age at first sexual act have both been associated with increased risk. Women who have had multiple pregnancies and are younger at the time of their first full-term pregnancy also demonstrate an increased risk. Long term use of oral contraceptives has been shown to increase risk in some studies, but this remains controversial. A 2007 study suggests that ongoing use of oral contraceptives raised the risk of cervical cancer but the risk diminishes when use of the contraceptives is stopped. ⁽⁵⁾

Because HPV is a sexually transmitted disease, behaviors that increase sexual contacts are considered risk factors. ⁽⁶⁾

Socioeconomic Status:
Low socioeconomic status has proven to be a significant risk factor for invasive cervical cancer due to its large impact on education and medical resources. Results of the analysis of several epidemiological studies indicate that Hispanic and African-American women have a higher risk of invasive cervical cancer than Caucasian women. ⁽⁷⁾

Decreased risk is associated with increased education--women without a college degree have an increased risk, regardless of race. Therefore, it is possible that if access to screening and medical education were equalized, race would not prove to be a significant risk factor. The increased risk with low socioeconomic status is attributed to a lack of screening, failure to treat precancerous conditions, and lack of knowledge about prevention of HPV infection.⁽¹⁾

Smoking:
Current smoking is a risk factor for the development cervical cancer due to the ability of carcinogens in cigarette smoke to cause mutations in DNA. In the epidemiological studies that have been conducted, smoking was associated with an increased risk of squamous cell carcinoma of the cervix, but not adenocarcinoma. ⁽¹⁾

Human Immunodeficiency Virus (HIV):
Women infected with HIV have been shown to have a five-fold risk of developing cervical cancer. HIV weakens the immune system, decreasing the ability to fight infection; therefore HPV infections are more likely to persist. This is thought to provide more time for the HPV to induce cancer. The high correlation between HIV infection and HPV infection is also partly due to the fact that both are sexually transmitted diseases and behaviors that put women at risk for one also put them at risk for the other. ⁽⁸⁾

In Utero Diethylstilbestrol (DES) Exposure:
DES is a synthetic estrogen used from the 1930s to the 1970s to reduce complications during pregnancy. Use of this drug was discontinued after it was demonstrated that the drug could harm the developing baby. Elevated risk of cervical cancer is just one of the potential health effects for women who where exposed to DES while they were in their mothers womb; others include a variety of gynecological cancers, reproductive tract irregularities, infertility and complications during pregnancy. ⁽⁹⁾

For more information about cervical cancer visit the Winship Cancer Institute of Emory University.

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