TY - JOUR
T1 - Oral alpha, beta, and gamma HPV types and risk of incident esophageal cancer
AU - Agalliu, Ilir
AU - Chen, Zigui
AU - Wang, Tao
AU - Hayes, Richard B.
AU - Freedman, Neal D.
AU - Gapstur, Susan M.
AU - Burk, Robert D.
N1 - Funding Information:
The American Cancer Society supports the follow-up and maintenance of the Cancer Prevention Studies, and would like to acknowledge the contribution to the Cancer Prevention Studies from central cancer registries supported through the Centers for Disease Control and Prevention's National Program of Cancer Registries and cancer registries supported by the National Cancer Institute's Surveillance Epidemiology and End Results Program. The NCI funded the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, which was also supported by contracts from the Division of Cancer Prevention of the NCI and by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics, NCI, NIH, Department of Health and Human Services. We would also like to thank the PLCO Cancer Screening Trial investigators and the staff from Information Management Services Inc. and Westat Inc. Most importantly, we thank the study participants for their contributions that made this study possible. This research was supported primarily by Public Health Service grant R21-CA152785 (to R.D. Burk and I. Agalliu), and in part by the Einstein Cancer Research Center grant (P30-CA013330), which were both funded by the NCI, NIH. Although some of the coauthors are employees of the American Cancer Society and the NIH, which fund and maintain data collection and management for the CPS-II NC and PLCO cohorts, the funding agencies had no role in the design and conduct of this study, data analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Drs. Agalliu and Burk had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Funding Information:
The American Cancer Society supports the follow-up and maintenance of the Cancer Prevention Studies, and would like to acknowledge the contribution to the Cancer Prevention Studies from central cancer registries supported through the Centers for Disease Control and Prevention's National Program of Cancer Registries and cancer registries supported by the National Cancer Institute's Surveillance Epidemiology and End Results Program. The NCI funded the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, which was also supported by contracts from the Division of Cancer Prevention of the NCI and by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics, NCI, NIH, Department of Health and Human Services. We would also like to thank the PLCO Cancer Screening Trial investigators and the staff from Information Management Services Inc. and Westat Inc. Most importantly, we thank the study participants for their contributions that made this study possible. This research was supported primarily by Public Health Service grant R21-CA152785 (to R.D. Burk and I. Agalliu), and in part by the Einstein Cancer Research Center grant (P30-CA013330), which were both funded by the NCI, NIH. Although some of the coauthors are employees of the American Cancer Society and the NIH, which fund and maintain data collection and management for the CPS-IINCandPLCOcohorts, the funding agencies had no role in the design and conduct of this study, data analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Drs. Agalliu and Burk had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Publisher Copyright:
© 2018 American Association for Cancer Research.
PY - 2018/10
Y1 - 2018/10
N2 - Background: Several studies have examined association between human papillomaviruses (HPV) and esophageal cancer, but results have been inconsistent. This is the first prospective study to investigate associations between α, β and γ HPV detection in the oral cavity and risk of esophageal cancer. Methods:Weconducted a nested case-control study among 96,650 cancer-free participants in the American Cancer Society Cancer Prevention Cohort and the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Incident esophageal cancer cases (n = 125) were identified during an average 3.9 years of follow-up. Three controls per case (n = 372) were selected and matched on age, sex, race/ethnicity, and time since mouthwash collection. α, β, and γ HPV DNA in oral samples were detected using a next-generation sequencing assay. Conditional logistic regression models were used to estimate OR and 95% confidence intervals (CIs), adjusting for smoking and alcohol consumption. Statistical significance was evaluated using permutation test. Results: Prevalence of oral α, β, and γ HPV was 18.4%, 64.8%, and 42.4% in cases and 14.3%, 55.1%, and 33.6% in controls, respectively. Oral HPV16 detection was not associated with esophageal cancer (OR = 0.54, 95% CI, 0.1-4.84) and none of the esophageal squamous cell carcinoma cases (n=28) wereHPV16 positive. Some oralHPVtypes were more common in cases than controls; however, none of the associations were statistically significant. Conclusions: Although HPVs in the oral cavity are very common, this study showed no evidence of association between oral HPVs and esophageal cancer. Impact: Oral HPVs may not contribute to risk of esophageal cancer.
AB - Background: Several studies have examined association between human papillomaviruses (HPV) and esophageal cancer, but results have been inconsistent. This is the first prospective study to investigate associations between α, β and γ HPV detection in the oral cavity and risk of esophageal cancer. Methods:Weconducted a nested case-control study among 96,650 cancer-free participants in the American Cancer Society Cancer Prevention Cohort and the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Incident esophageal cancer cases (n = 125) were identified during an average 3.9 years of follow-up. Three controls per case (n = 372) were selected and matched on age, sex, race/ethnicity, and time since mouthwash collection. α, β, and γ HPV DNA in oral samples were detected using a next-generation sequencing assay. Conditional logistic regression models were used to estimate OR and 95% confidence intervals (CIs), adjusting for smoking and alcohol consumption. Statistical significance was evaluated using permutation test. Results: Prevalence of oral α, β, and γ HPV was 18.4%, 64.8%, and 42.4% in cases and 14.3%, 55.1%, and 33.6% in controls, respectively. Oral HPV16 detection was not associated with esophageal cancer (OR = 0.54, 95% CI, 0.1-4.84) and none of the esophageal squamous cell carcinoma cases (n=28) wereHPV16 positive. Some oralHPVtypes were more common in cases than controls; however, none of the associations were statistically significant. Conclusions: Although HPVs in the oral cavity are very common, this study showed no evidence of association between oral HPVs and esophageal cancer. Impact: Oral HPVs may not contribute to risk of esophageal cancer.
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U2 - 10.1158/1055-9965.EPI-18-0287
DO - 10.1158/1055-9965.EPI-18-0287
M3 - Article
C2 - 30087123
AN - SCOPUS:85054402104
VL - 27
SP - 1168
EP - 1175
JO - Cancer Epidemiology Biomarkers and Prevention
JF - Cancer Epidemiology Biomarkers and Prevention
SN - 1055-9965
IS - 10
ER -