4.7 Article

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

Journal

EUROPEAN JOURNAL OF CANCER
Volume 51, Issue 13, Pages 1732-1741

Publisher

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

Keywords

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

Categories

Funding

  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.

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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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