4.7 Article

Human papillomavirus genotype attribution for HPVs 6, 11, 16, 18, 31, 33, 45, 52 and 58 in female anogenital lesions

期刊

EUROPEAN JOURNAL OF CANCER
卷 51, 期 13, 页码 1732-1741

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.ejca.2015.06.001

关键词

Human papillomavirus; Uterine cervical neo-plasms; Anus neoplasms; Vulvar neoplasms; Vaginal neoplasms; Papillomavirus vaccines; Precancerous conditions

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资金

  1. Spanish public grants from Instituto de Salud Carlos III [FIS PI030240, FIS PI061246, RCESP C03/09, RTICESP C03/10, RTIC RD06/0020/0095, RD12/0036/0056, CIBERESP]
  2. Agencia de Gestio d'Ajuts Universitaris i de Recerca AGAUR [2005SGR00695, 2009SGR126, 2014SGR1077, 2014SGR2016]
  3. Marato de TV3 Foundation [051530]
  4. Lilly Foundation (Premio de Investigacion Biomedica Preclinica F. Xavier Bosch)
  5. GlaxoSmithKline Biologicals, Sanofi Pasteur MSD and Merck Co, Inc.

向作者/读者索取更多资源

Objective: Human 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). Methods: Estimations 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. Results: HPV 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. Conclusions: The 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. (C) 2015 Elsevier Ltd. All rights reserved.

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