ArticlesViral load of human papilloma virus 16 as a determinant for development of cervical carcinoma in situ: a nested case-control study
Introduction
Infection by certain types of human papillomavirus (HPV), especially HPV 16 and HPV 18, increases the risk of cervical cancer. Although HPV infection is common among young women, less than 1 % of those positive for oncogeneic types of HPV develop cervical cancer.1, 2 Therefore, the presence of HPV has a low predictive value. Several studies have suggested that the amount of HPV could be an important factor for progression from HPV infection to cervical cancer.3, 4, 5, 6, 7, 8, 9, 10 Without the availability of a method to estimate the amount of HPV in clinical samples, however, no study has been able to address the importance of viral load for cancer risk.
We did a nested case-control study of the relation between amount of HPV DNA and development of carcinoma in situ by analysis of archived cervical-smear samples.
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Patients
We studied samples collected during routine gynaecological health checks from women with cervical cancer and individually matched controls from the general population.11 We selected women from a cohort who lived in Uppsala County, Sweden, between 1969 and 1995.11 To identify all eligible cases of cervical carcinoma in situ, we merged information from the organised screening programme, recorded from 1969 to 1995, with data from the National Cancer Registry. We included women who met the
Results
The nested case-control study included 504 cases and 662 controls. For some controls, only one smear was available during the follow-up period. Therefore, a second matched control for each of those was randomly chosen from the original pool of controls to increase the statistical power. 158 second controls were included. To confirm the cancer diagnosis of cases, the histological samples (complete cone or small biopsy) were reassessed by an experienced pathologist. After cytological and
Discussion
High amounts of HPV 16 DNA is a major risk factor for development of cervical carcinoma in situ. The amount of viral DNA could vary between individuals because of environmental factors,11, 17, 18, 19, 20 genetic factors, or both. Several environmental factors, such as smoking, use of oral contraceptives, and sequence variation in oncogenic HPV types have been purported to affect the risk of infection. The amount of viral DNA may also reflect inherent differences between individuals in response
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