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.