Some studies have suggested that the presence in tumors of nucleic acids from human papillomavirus (HPV) constitutes a prognostic marker of disease severity in cervical cancer. There are two conflicting lines of evidence in this regard. First, the presence of HPV 18 is equated to rapid progression through early disease stages, possibly resulting in a more aggressive clinical course. Although fragmentary, in terms of the clinical and epidemiological basis, this line of evidence has some experimental support. Second, the absence of HPV from the tumor would confer a worse prognosis than if any viral types were present. Unlike the former, the latter line of evidence is not bolstered by experimental data but emerged from persuasive clinical studies, which had adequate sample sizes, used survival end points, and controlled for confounders. The absence of HPV in some tumors could indicate that they originated through different oncogenic mechanisms, perhaps resulting in different cell proliferation rates and, consequently, distinct clinical behavior. On the other hand, HPV detectability could simply be a correlate of other genuine prognostic characteristics, which would explain its association with survival. Both the nature and the mechanism of the prognostic role for HPV in cervical cancer remain to be elucidated. The paucity of studies can be attributed to the labor-intensive nature of assays for HPV. It is hoped that the advent of the polymerase chain reaction method will facilitate the conduct of retrospective studies of archival histopathology specimens and survival information.(ABSTRACT TRUNCATED AT 250 WORDS)

This content is only available via PDF.