Cell Cycle Checkpoint Control Is Bypassed by Human Papillomavirus Oncogenes
This extract was created in the absence of an abstract.
Excerpt
Although the incidence of invasive squamous cell cancer of the cervix has declined in Western countries because of the ability of Pap smear screening to detect premalignant lesions, cervical cancer remains the most common malignancy of women in underdeveloped countries. Both epidemiological and experimental studies clearly indicate that infection by certain high-risk papillomaviruses (HPVs) is a causal step in the development of the tumor (for review, see zur Hausen 1991). Approximately 90% of cervical cancers retain HPV DNA, and the E6 and E7 viral oncogenes are almost invariably expressed. Infection by papillomaviruses precedes the development of cancer by decades, and the tumors that develop have various cytogenetic abnormalities. In culture, the E6 and E7 genes of the cancer-associated HPVs, e.g., types 16 and 18, are able in combination to efficiently immortalize primary human keratinocytes; progression to tumorigenicity requires additional alterations in cellular genes. Thus, it is likely that HPV infection...
