Serologic Response to Oncogenic Human Papillomavirus Types in Male and Female University Students in Busan, South Korea

Clifford, Gary M.; Shin, Hai‐Rim; Oh, Jin Kyoung; Waterboer, Tim; Ju, Young-Hee; Vaccarella, Salvatore; Quint, Wim; Pawlita, Michael; Franceschi, Silvia

doi:10.1158/1055-9965.epi-07-0349

Cited by 112 publications

(116 citation statements)

References 38 publications

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“…Mean fluorescence intensity (MFI) values were dichotomized as antibody positive or negative, 8-11 using predefined cutoff values (Appendix Table A1 [online only]) based on the mean Ϯ 5 standard deviations (SD; for HPV early proteins) or the mean Ϯ 3 SDs excluding positive outliers (for HPV late proteins) of the MFI values derived from serum samples of 117 female, HPV DNA-negative, self-reported virgins from a cross-sectional study among Korean students. 13 Values below 200 MFI were set to this minimum cutoff. For HPV6 E6, HPV11 L1, and HPV33 E7, an arbitrarily defined cutoff of 500 MFI was used.…”

Section: Serologic Analysesmentioning

confidence: 99%

Evaluation of Human Papillomavirus Antibodies and Risk of Subsequent Head and Neck Cancer

Kreimer

Johansson

Waterboer

et al. 2013

JCO

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287

350

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A B S T R A C T PurposeHuman papillomavirus type 16 (HPV16) infection is causing an increasing number of oropharyngeal cancers in the United States and Europe. The aim of our study was to investigate whether HPV antibodies are associated with head and neck cancer risk when measured in prediagnostic sera. MethodsWe identified 638 participants with incident head and neck cancers (patients; 180 oral cancers, 135 oropharynx cancers, and 247 hypopharynx/larynx cancers) and 300 patients with esophageal cancers as well as 1,599 comparable controls from within the European Prospective Investigation Into Cancer and Nutrition cohort. Prediagnostic plasma samples from patients (collected, on average, 6 years before diagnosis) and control participants were analyzed for antibodies against multiple proteins of HPV16 as well as HPV6, HPV11, HPV18, HPV31, HPV33, HPV45, and HPV52. Odds ratios (ORs) of cancer and 95% CIs were calculated, adjusting for potential confounders. All-cause mortality was evaluated among patients using Cox proportional hazards regression. Results HPV16E6 seropositivity was present in prediagnostic samples for 34.8% of patients with oropharyngeal cancer and 0.6% of controls (OR, 274; 95% CI, 110 to 681) but was not associated with other cancer sites. The increased risk of oropharyngeal cancer among HPV16 E6 seropositive participants was independent of time between blood collection and diagnosis and was observed more than 10 years before diagnosis. The all-cause mortality ratio among patients with oropharyngeal cancer was 0.30 (95% CI, 0.13 to 0.67), for patients who were HPV16 E6 seropositive compared with seronegative. ConclusionHPV16 E6 seropositivity was present more than 10 years before diagnosis of oropharyngeal cancers. J Clin Oncol 31:2708-2715. © 2013 by American Society of Clinical Oncology INTRODUCTIONHuman papillomavirus type 16 (HPV16) is recognized as a cause of virtually all cervical cancers and of a substantial proportion of other anogenital cancers and oropharyngeal cancers. 1 The association between HPV16 and cancers of the oral cavity and larynx is less clear but, if associated, the attributable proportion is small. 1 HPV16 has been associated with a rapid increase in the incidence of oropharynx cancer in some parts of the world, notably in the United States, Sweden, and Australia, where it is now responsible for more than 50% of cases.2-4 If current trends continue, the annual number of oropharyngeal cancers in the United States may soon surpass the number of cervical cancers. 2The only evidence for the temporal relationship between HPV exposure and development of head and neck cancers (HNC) comes from a study within the Nordic serum banks linked to tumor registries: a significant 14-fold increased risk for cancer of the oropharynx was reported for seropositivity to the L1 capsid protein of HPV16.5 Antibodies against HPV L1 represent cumulative past HPV infection from multiple possible anatomic sites (ie, genital, anal, or oral), are common in controls, and © 2013 by American Society o...

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Section: Serologic Analysesmentioning

confidence: 99%

Evaluation of Human Papillomavirus Antibodies and Risk of Subsequent Head and Neck Cancer

Kreimer

Johansson

Waterboer

et al. 2013

JCO

Self Cite

287

350

View full text Add to dashboard Cite

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“…7 Antibody reactivity was quantitatively expressed in Median Fluorescence Intensity (MFI) units, and MFI values were dichotomized as antibody-positive or antibodynegative, using seropositivity cutoffs which were HPV typespecific and defined previously. 8 For the nested case-control analyses, HPV L1 seropositivity refers to that for at least one of the nine HPV types analyzed, and high-risk HPV L1 seropositivity refers to positivity for at least one of the eight high-risk HPV types analyzed.…”

Section: Serological Testingmentioning

confidence: 99%

Smoking as a major risk factor for cervical cancer and pre-cancer: Results from the EPIC cohort

et al. 2014

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A total of 308,036 women were selected from the European Prospective Investigation into Cancer and Nutrition (EPIC) study to evaluate the association between tobacco smoking and the risk of cervical intraepithelial neoplasia of grade 3 (CIN3)/carcinoma in situ (CIS) and invasive cervical cancer (ICC). At baseline, participants completed a questionnaire and provided blood samples. During a mean follow‐up time of 9 years, 261 ICC cases and 804 CIN3/CIS cases were reported. In a nested case–control study, the baseline sera from 609 cases and 1,218 matched controls were tested for L1 antibodies against HPV types 11, 16, 18, 31, 33, 35, 45, 52, 58, and antibodies against Chlamydia trachomatis (CT), and Human Herpes Virus 2 (HHV‐2). Cervical samples were not available for HPV‐DNA analysis in this study. Multivariate analyses were used to estimate associations between smoking and risk of CIN3/CIS and ICC in the cohort and the case–control studies. In the cohort analyses smoking status, duration and intensity showed a two‐fold increased risk of CIN3/CIS and ICC, while time since quitting was associated with a two‐fold reduced risk. In the nested case–control study, consistent associations were observed after adjustment for HPV, CT and HHV‐2 serostatus, in both HPV seronegative and seropositive women. Results from this large prospective study confirm the role of tobacco smoking as an important risk factor for both CIN3/CIS and ICC, even after taking into account HPV exposure as determined by HPV serology. The strong beneficial effect of quitting smoking is an important finding that will further support public health policies for smoking cessation.

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“…In total, plasma samples from 4,328 controls and 3,083 lung cancer cases were tested using the bead-based multiplex serology method described elsewhere (20). Serology data were dichotomized on the basis of study-specific cutoffs derived using a set of known reference sera (21,22). Thresholds derived for the prospective study, which were higher in general, were applied to the retrospective studies to allow for comparisons.…”

Section: Hpv Serologymentioning

confidence: 99%

No Causal Association Identified for Human Papillomavirus Infections in Lung Cancer

Anantharaman¹,

Gheit²,

Waterboer

et al. 2014

Cancer Research

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Human papillomavirus (HPV) infections have been implicated in lung carcinogenesis, but causal associations remain uncertain. We evaluated a potential causal role for HPV infections in lung cancer through an analysis involving serology, tumor DNA, RNA, and p16 protein expression. Association between type-specific HPV antibodies and risk of lung cancer was examined among 3,083 cases and 4,328 controls in two case-control studies (retrospective) and one nested case-control study (prospective design). Three hundred and thirty-four available tumors were subjected to pathologic evaluation and subsequent HPV genotyping following stringent conditions to detect all high-risk and two low-risk HPV types. All HPV DNA-positive tumors were further tested for the expression of p16 protein and type-specific HPV mRNA. On the basis of the consistency of the results, although HPV11 and HPV31 E6 antibodies were associated with lung cancer risk in the retrospective study, no association was observed in the prospective design. Presence of type-specific antibodies correlated poorly with the presence of the corresponding HPV DNA in the tumor. Although nearly 10% of the lung tumors were positive for any HPV DNA (7% for HPV16 DNA), none expressed the viral oncogenes. No association was observed between HPV antibodies or DNA and lung cancer survival. In conclusion, we found no supportive evidence for the hypothesized causal association between HPV infections and lung cancer. Cancer Res; 74(13); 3525-34. Ó2014 AACR.

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Serologic Response to Oncogenic Human Papillomavirus Types in Male and Female University Students in Busan, South Korea

Cited by 112 publications

References 38 publications

Evaluation of Human Papillomavirus Antibodies and Risk of Subsequent Head and Neck Cancer

Evaluation of Human Papillomavirus Antibodies and Risk of Subsequent Head and Neck Cancer

Smoking as a major risk factor for cervical cancer and pre-cancer: Results from the EPIC cohort

No Causal Association Identified for Human Papillomavirus Infections in Lung Cancer

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