Human papillomavirus genotype attribution for HPVs 6, 11, 16, 18, 31, 33, 45, 52 and 58 in female anogenital lesions |
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| Institution: | 1. Department of Gynecologic Oncology, University “Sapienza”, Viale del Policlinico 155, 00161 Rome, Italy;2. Service of Biostatistics, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy;3. Department of Gynecologic Oncology, University “Campus Biomedico”, Via Alvaro del Portillo 21, 00128 Rome, Italy;1. Department of Obstetrics and Gynecology, Division General Gynecology and Gynecologic Oncology, Medical University of Vienna, Austria;2. Karl Landsteiner Institute for General Gynecology and Experimental Gynecologic Oncology, Austria;3. Department of Obstetrics and Gynecology, Medical University Hannover, Germany;4. Department of Obstetrics and Gynecology, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany;5. Onkologisches Therapiezentrum am Krankenhaus Jerusalem, Hamburg, Germany;6. Department of Gynecology and Obstetrics, University Hospital Ulm, Ulm, Germany;7. Department of Gynecology, Johannes Gutenberg University Medical Center, Mainz, Germany;8. Department of Obstetrics and Gynecology, University Hospital Freiburg, Germany;9. Department of Gynecology, European Competence Center for Ovarian Cancer, Campus Virchow Klinikum, Charité - Universitätsmedizin Berlin, Germany;10. Department of Gynecology, University of Halle, Halle, Germany;11. Department of Gynecology, Klinikum Ludwigshafen, Ludwigshafen, Germany;12. Department of Gynecology, Obstetris University Hospital Marburg, Marburg, Germany;13. Department of Gynecology, Alb Fils Kliniken, Klinik am Eichert, Goeppingen, Department of Gynecology, University Hospital Erlangen, Germany;14. Department of Gynecology, University Medicine of Greifswald, Greifswald, Germany;15. Department of Gynecology, Kliniken Essen Mitte, Essen, Germany;p. Department of Gynecology and Obstetrics, Technische Universität Dresden, TU Dresden, Dresden, Department of Gynecology and Obstretrics, University Hospital Essen, Germany;q. Department of Gynaecology and Gynaecologic Oncology, University Medical Center Hamburg-Eppendorf, Germany;1. INSERM, U1153 Paris, France;2. CHRU de Tours, Department of Cancer Screening, Tours, France;3. CHRU de Tours, INSERM CIC 0202, Tours, France;4. Université François-Rabelais de Tours, PRES Centre-Val de Loire Université, Tours, France;5. INSERM U966, Tours, France;6. CHRU de Tours, Department of Bacteriology and Virology, Tours, France;7. Institut inter-Régional pour la Santé (IRSA), Tours, France;8. CHRU de Tours, Birth Control Care Center, Tours, France;9. CHRU de Tours, Department of Gynecology and Obstetrics, Tours, France |
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| Abstract: | ObjectiveHuman papillomavirus (HPV) vaccines can potentially control cervical cancer and help to reduce other HPV-related cancers. We aimed to estimate the relative contribution (RC) of the nine types (HPVs 16/18/31/33/45/52/58/6/11) included in the recently approved 9-valent HPV vaccine in female anogenital cancers and precancerous lesions (cervix, vulva, vagina and anus).MethodsEstimations were based on an international study designed and coordinated at the Catalan Institute of Oncology (Barcelona-Spain), including information on 10,575 invasive cervical cancer (ICC), 1709 vulvar, 408 vaginal and 329 female anal cancer cases and 587 Vulvar Intraepitelial Neoplasia grade 2/3 (VIN2/3), 189 Vaginal Intraepitelial Neoplasia grade 2/3 (VaIN2/3) and 29 Anal Intraepitelial Neoplasia grade 2/3 (AIN2/3) lesions.Consecutive histologically confirmed paraffin-embedded cases were obtained from hospital pathology archives from 48 countries worldwide. HPV DNA-detection and typing was performed by SPF10-DEIA-LiPA25 system and RC was expressed as the proportion of type-specific cases among HPV positive samples. Multiple infections were added to single infections using a proportional weighting attribution.ResultsHPV DNA prevalence was 84.9%, 28.6%, 74.3% and 90.0% for ICC, vulvar, vaginal and anal cancers, respectively, and 86.7%, 95.8% and 100% for VIN2/3, VaIN2/3 and AIN2/3, respectively. RC of the combined nine HPV types was 89.5% (95% confidence interval (CI): 88.8–90.1)-ICC, 87.1% (83.8–89.9)-vulvar, 85.5% (81.0–89.2)-vaginal, 95.9% (93.0–97.9)-female anal cancer, 94.1% (91.7–96.0)-VIN2/3, 78.7% (71.7–84.2)-VaIN2/3 and 86.2% (68.3–96.1)-AIN2/3. HPV16 was the most frequent type in all lesions. Variations in the RC of HPVs 31/33/45/52/58 by cancer site were observed, ranging from 7.8% (5.0–11.4)-female anal cancer to 20.5% (16.1–25.4)-vaginal cancer.ConclusionsThe addition of HPVs 31/33/45/52/58 to HPV types included in current vaccines (HPV16/18) could prevent almost 90% of HPV positive female anogenital lesions worldwide. Taking into account that most HPV-related cancers are ICC ones, the 9-valent HPV vaccine could potentially avoid almost 88% of all female anogenital cancers. |
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| Keywords: | Human papillomavirus Uterine cervical neoplasms Anus neoplasms Vulvar neoplasms Vaginal neoplasms Papillomavirus vaccines Precancerous conditions |
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