Basic Principles of Cervical Cancer Control

The vast majority of cervical cancer cases are caused by HPV, a sexually transmitted agent that infects the cells of the cervix and slowly causes cellular changes that can result in cancer.3 A 1999 study estimated that over 99 percent of cervical cancers worldwide contained HPV DNA.4 Women generally are infected with HPV in their teens, twenties, or thirties, although cervical cancer can develop 20 years or more after HPV infection (see Figure 2). Various studies have looked at other risk factors associated with cervical cancer, including sexual activity, obstetric history, and health behaviors (such as smoking and nutrition). Most of these factors probably are proxies for HPV infection, although smoking, parity, and perhaps nutritional status likely are independent cofactors in HPV progression.

The pathway to preventing cervical cancer deaths is simple and effective. If the precancerous changes in cervical tissue (which can linger for years) are identified and successfully treated, the lesions will not develop into cervical cancer. Treating the abnormal, dysplastic tissue also seems to protect women from developing cervical cancer in the future.5

Screening and dysplasia treatment are cost-effective interventions when compared to expensive, often futile hospital-based treatment of invasive cancer. A World Bank analysis suggested that, in 1993, cervical cancer screening (defined as screening women every five years, with standard follow-up for identified cases) cost about US$100 per disability-adjusted life year (DALY) gained, compared with about US$2,600 per DALY for treatment of invasive cancer and palliative care.6 

Of course primary prevention of cervical cancer through preventing HPV infection also will contribute to reducing cancer mortality. Primary prevention of HPV presents greater challenges than prevention of most other sexually transmitted infections (STIs), however. HPV generally is asymptomatic and easily transmitted. While treatments for the genital warts caused by some types of HPV are available, there are no therapies that eliminate the underlying infection. The virus can remain infectious for years and can exist throughout most of the anogenital area (including areas not covered by condoms). The standard STI prevention recommendations (for example, regular use of condoms or other barrier methods and reducing the number of sexual partners) may help women reduce the chance of HPV infection, but the degree to which they will affect the overall incidence of cervical cancer is unclear. 

A more promising approach to primary prevention—vaccines against HPV—is some years away. A number of private companies and public-sector agencies worldwide are exploring various candidate HPV vaccines. While research to date is encouraging, much remains to be clarified regarding the safety, effectiveness, and program implications of potential HPV vaccines.7

It is important to take into account the current understanding of the natural history of cervical cancer in deciding when to initiate screening, how often to screen, and when to recommend treatment and/or follow-up evaluation (see Figure 2).

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When to initiate screening: Cervical cancer most often develops in women after age 40, and high-grade dysplasia generally is detectable up to 10 years before cancer develops, with a peak dysplasia rate at about age 35. Therefore, where program sources are limited, screening initially should focus on women in their thirties and forties.

How often to screen: Cervical cancer generally develops slowly from precursor lesions; therefore, screening can take place relatively infrequently and still have a significant impact on morbidity and mortality. Screening every three years has almost as great an impact as screening every year. Even screening every 10 years or once in a lifetime can have a significant impact.8,9 The emphasis of screening programs, therefore, should be on coverage of high-risk women rather than on frequency (see Table 1).

Whom to treat and follow up: Because most low-grade dysplasia regresses spontaneously, treatment generally should focus on high-grade dysplasia, with follow-up mechanisms in place for women with lower-grade lesions. About one-third of untreated high-grade lesions will progress to cancer within 10 years, whereas approximately 70 percent of low-grade dysplasia regresses spontaneously or does not progress.10,11