Abstract
BackgroundHPV16 variants are associated with different risks for development of CIN3 and invasive cancer, although all are carcinogenic. The relationship of HPV 16 variants to cancer survival has not been studied.Methods155 HPV16-positive cervical cancers were categorized according to European and non-European variant patterns by DNA sequencing of the E6 open reading frame. Clinico-pathologic parameters and clinical outcome were collected by chart review and death registry data.ResultsOf the 155 women (mean age 44.7 years; median follow-up 26.7 months), 85.2% harbored European variants while 14.8% had non-European sequences. HPV16 variants differed by histologic cell type (p = 0.03) and stage (1 vs. 2+; p = 0.03). Overall, 107 women (68.0%) were alive with no evidence of cancer, 42 (27.1%) died from cervical cancer, 2 (1.3%) were alive with cervical cancer, and 4 (2.6%) died of other causes. Death due to cervical cancer was associated with European variant status (p < 0.01). While 31% of women harboring tumors with European variants died from cervical cancer during follow-up, only 1 of 23 (4.4%) non-European cases died of cancer. The better survival for non-European cases was partly mediated by lower stage at diagnosis.ConclusionsOverall, invasive cervical cancers with non-European variants showed a less aggressive behavior than those with European variants. These findings should be replicated in a population with more non-European cases.
Highlights
HPV16 variants are associated with different risks for development of CIN3 and invasive cancer, all are carcinogenic
We have previously reported the patterns of HPV16 variants in the spectrum of cervical lesions in our population [11]
While our study confirmed the increased risk for progression to carcinoma associated with 16-NE variants, 16-E patterns were found in the majority of HPV16 lesions, including cancers
Summary
HPV16 variants are associated with different risks for development of CIN3 and invasive cancer, all are carcinogenic. HPV variants are defined as isolates with primary DNA sequence differences that total no more than 2% of the L1 open. We have previously reported the patterns of HPV16 variants in the spectrum of cervical lesions in our population [11]. While our study confirmed the increased risk for progression to carcinoma associated with 16-NE variants, 16-E patterns were found in the majority of HPV16 lesions, including cancers. We attributed this to the dominance of the 16-E patterns in our population and to the fact that all major variant categories can be found in cancers
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