In yesterday’s plenary session, Denise Galloway, PhD, of the Fred Hutchinson Cancer Center in Seattle, WA, described how the discovery that human papillomavirus (HPV) causes cervical cancer led to the development of the HPV vaccine within a mere 30 years. HPVs are a large family of viruses that are associated with a range of cancers, including cervical, anogenital, mouth, and throat cancer.
Galloway began the session by explaining that HPV is found in all cervical cancers, nearly all anogenital cancers, and in half of oral cancers. According to the CDC, HPV causes over 30,000 cases of cancer each year within the United States. World-wide there are an estimated 530,000 cases of cervical cancer per year and 275,000 deaths per year.
Galloway has been studying HPV and its association with cancer since the early 1980s. Her laboratory and collaborators demonstrated that HPV is associated with cervical cancer, with HPV 16 and HPV 18 found in 50% and 20% of these cancers, respectively. The remaining 30% of cancers are due to nearly a dozen other types of HPV.
To date, more than 100 strains of HPV have been identified with more than 30 strains found to infect the genital tract. These can be subdivided into high-risk HPV and low-risk HPV strains. The high-risk HPV strains are found in cervical cancers, whereas the low-risk HPV strains do not progress into cancer.
Next, she presented an overview of the natural history of genital HPV infection including the progression of how HPV infects cervical cells. In most cases, the active infection is resolved, but in some cases, the atypical cells progress into precancerous lesions which can lead to cervical cancer. The greatest risk factor for progression is the failure of cervical screening, which historically relied on Pap testing. Screening allows for treatment of precancerous lesions before they can progress to cancer.
Fortunately, cancer usually does not develop for approximately three decades after the time of infection, which is why early intervention and screening programs have been particularly successful in preventing cancer progression.
Galloway then explained the development of vaccines to prevent HPV infection. In June 2006, FDA approved the first vaccine for HPV infection that protects against HPV 6, 11, 16, and 18. Clinical studies of this vaccine demonstrated nearly 100% efficacy in preventing HPV infection.
This was just the second vaccine available to prevent cancer, following approval of the hepatitis B vaccine in 1981. Currently, there are three commercially available vaccines. The vaccines have caused a rapid decrease in the HPV prevalence rate among women.
Despite the many successes in moving from virus to vaccine during a comparatively short time, the story is not quite finished. Substantial work remains to provide widespread vaccination of males to prevent HPV transmission and reduce mouth and throat cancer.
Galloway also presented ongoing work aimed at improving global availability of the vaccine, including the inclusion of other high-risk HPV strains and optimizing the frequency of boosters. She described how increasing both screening and vaccination rates world-wide remain necessary to reduce the incidence of cervical cancer over the next 60 years.