Persistence of Type-Specific Human Papillomavirus Infection among Cytologically Normal Women

Hildesheim, Allan; Schiffman, Mark; Gravitt, Patti E.; Glass, Andrew G.; Greer, Catherine E.; Zhang, Tracy; Scott, David; Rush, Brenda B.; Lawler, Patricia; Sherman, Mark E.; Kurman, Robert J.; Manos, M. Michele

doi:10.1093/infdis/169.2.235

Cited by 621 publications

(426 citation statements)

References 19 publications

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“…HPV infection wanes due to clearance, resulting in a decreased subsequent cancer risk over an extended period of time [26,27]. This may explain our finding that cervical cancer survivors are at the greatest risk of a subsequent malignancy for up to 15 years post cancer diagnosis.…”

Section: Discussionmentioning

confidence: 98%

Cervical cancer survivors at increased risk of subsequent tobacco-related malignancies, United States 1992–2008

Underwood

Rim

Fairley

et al. 2012

Cancer Causes Control

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Purpose-Persistent smoking among cancer survivors may increase their risk of subsequent malignancies, including tobacco-related malignancies. Despite these risks, nearly 40 % of women diagnosed with cervical cancer continue to smoke after diagnosis. This study describes the relative risk of developing any subsequent and tobacco-related malignancy among cervical cancer survivors.Methods-We examined data from the year 1992 to 2008 in 13 Surveillance, Epidemiology and End Results registries. We calculated the standardized incidence ratio (SIR) and 95 % confidence limits (CLs) for all subsequent and tobacco-related malignancies among cervical cancer survivors. Tobacco-related malignancies were defined according to the 2004 Surgeon General's Report on the Health Consequences of Smoking. For comparison with cervical cancer survivors, SIRs for subsequent malignancies were also calculated for female survivors of breast or colorectal cancers.Results-The SIR of developing a subsequent tobacco-related malignancy was higher among cervical cancer survivors (SIR = 2.2, 95 % CL = 2.0-2.4). Female breast (SIR = 1.1, 95 % CL = 1.0-1.1) and colorectal cancer survivors (1.1, 1.1-1.2) also had an elevated risk. The increased risk of a subsequent tobacco-related malignancy among cervical cancer survivors was greatest in the first 5 years after the initial diagnosis and decreased as time since diagnosis elapsed.Conclusion-Women with cervical cancer have a two-fold increased risk of subsequent tobacco-related malignancies, compared with breast and colorectal cancer survivors. In an effort to decrease their risk of subsequent tobacco-related malignancies, cancer survivors should be targeted for tobacco prevention and cessation services. Special attention should be given to cervical cancer survivors whose risk is almost twice that of breast or colorectal cancer survivors.

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Section: Discussionmentioning

confidence: 98%

Cervical cancer survivors at increased risk of subsequent tobacco-related malignancies, United States 1992–2008

Underwood

Rim

Fairley

et al. 2012

Cancer Causes Control

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“…This could represent false negative HPV DNA tests due to old tissue samples or samples of bad quality. Since most of the HPV infections are transient (Hildesheim et al, 1994;Evander et al, 1995;Ho et al, 1998), another possibility is that after the infections with HPV 16, 18 and/or 33 have ceased, a history of HPV infection may still increase the risk for cervical carcinoma. However, as seropositive women were not at increased risk to develop carcinomas that were HPV-negative or containing other types of virus, our data strongly suggests that persistent type-specific HPV infection is required and that the HPV DNA-negative cases either really are HPV-negative or contain unknown HPV types that are not adequately amplified by the PCR tests used.…”

Section: Discussionmentioning

confidence: 99%

A prospective study of the relationship between prediagnostic Human Papillomavirus seropositivity and HPV DNA in subsequent cervical carcinomas

et al. 2002

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Several prospective studies with invasive carcinoma as endpoint have supported Human Papillomavirus as a cause of cervical carcinoma. However, the largest study used seroepidemiology and did not analyse presence of Human Papillomavirus DNA in the subsequent tumour. Linkage of serum bank registries and cancer registries had identified 196 women with a registered cervical carcinoma after donation of a serum sample. For the present study, biopsies for 127 cases could be located, verified to contain invasive carcinoma and be amplified by PCR. Three control women who had remained alive and without cervical carcinoma during an equal length of follow-up had been matched to each of the case women and tested for HPV antibodies. Presence of Human Papillomavirus DNA in the tumours was analysed by general primer and type specific PCR. HPV16-seropositive women had a relative risk of 4.4 (95% CI: 2.2 -8.8) to develop cervical carcinoma carrying HPV16 DNA. By contrast, there was no excess risk for Human Papillomavirus 16-seropositive women to develop cervical carcinoma devoid of HPV16 DNA. Prediagnostic HPV16 seropositivity was strongly correlated with later HPV16 DNA positivity of the tumour (P50.001) and prediagnostic HPV18 seropositivity correlated with HPV18 DNA in the tumour (P50.03). The link between prediagnostic seropositivity and type of viral DNA in the cancer implies that the carcinogenic effect of infection with these viruses is dependent on persistent presence of type-specific viral DNA. The most important risk factor for development of cervical carcinoma is infection with the oncogenic types of human papillomavirus (HPV). A series of cross-sectional case-control studies, based both on HPV DNA testing of tumours (Walboomers et al, 1999), measurement of serum HPV antibodies (Dillner et al, 1995), or both (Nonnenmacher et al, 1995;de Sanjose et al, 1996) have found a consistent and strong association between HPV and cervical carcinoma.That the association between HPV and cervical carcinoma is causal is supported also by prospective studies, both with cervical intraepithelial neoplasia (Koutsky et al, 1992;Chua et al, 1996) and invasive cervical carcinoma as the end-point Shah et al, 1997;Vonka et al, 1999;Wallin et al, 1999). However, most prospective studies are based on limited numbers of cases. The largest study to date is a seroepidemiological study that contained 182 cases (Dillner et al, 1997). However, prediagnostic seropositivity and type of HPV DNA in subsequently occurring invasive carcinoma has not been previously performed. Combining seroepidemiological studies with HPV DNA analyses in prospective studies could be important for several reasons. For example, there are indications that prior or ongoing HPV infections may interact in a complex fashion in cervical carcinogenesis (Luostarinen et al, 1999;Silins et al, 1999). By comparing prediagnostic assessment of virus exposure with presence of virus DNA in the tumour, it could be possible to infer whether type-specific persistence of HPV is the predominant...

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“…17,23 We used three different methods, all of which generated the same conclusions. For this presentation, we have presented the consensus primer PCR test results for oncogenic types of HPV.…”

Section: Hpv Dna Testingmentioning

confidence: 99%

Use of human papillomavirus DNA testing to compare equivocal cervical cytologic interpretations in the United States, Scandinavia, and the United Kingdom

Scott

Hagmar²,

Maddox³

et al. 2002

Cancer

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Persistence of Type-Specific Human Papillomavirus Infection among Cytologically Normal Women

Cited by 621 publications

References 19 publications

Cervical cancer survivors at increased risk of subsequent tobacco-related malignancies, United States 1992–2008

Cervical cancer survivors at increased risk of subsequent tobacco-related malignancies, United States 1992–2008

A prospective study of the relationship between prediagnostic Human Papillomavirus seropositivity and HPV DNA in subsequent cervical carcinomas

Use of human papillomavirus DNA testing to compare equivocal cervical cytologic interpretations in the United States, Scandinavia, and the United Kingdom

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