BACKGROUND: Human papillomavirus (HPV) contribution in vulvar intraepithelial lesions (VIN) and invasive vulvar cancer (IVC) is not clearly established. This study provides novel data on HPV markers in a large series of VIN and IVC lesions. METHODS: Histologically confirmed VIN and IVC from 39 countries were assembled at the Catalan Institute of Oncology (ICO). HPV-DNA detection was done by polymerase chain reaction using SPF-10 broad-spectrum primers and genotyping by reverse hybridisation line probe assay (LiPA25) (version 1). IVC cases were tested for p16(INK4a) by immunohistochemistry (CINtec histology kit, ROCHE). An IVC was considered HPV driven if both HPV-DNA and p16(INK4a) overexpression were observed simultaneously. Data analyses included algorithms allocating multiple infections to calculate type-specific contribution and logistic regression models to estimate adjusted prevalence (AP) and its 95% confidence intervals (CI). RESULTS: Of 2296 cases, 587 were VIN and 1709 IVC. HPV-DNA was detected in 86.7% and 28.6% of the cases respectively. Amongst IVC cases, 25.1% were both HPV-DNA and p16(INK4a) positive. IVC cases were largely keratinising squamous cell carcinoma (KSCC) (N=1234). Overall prevalence of HPV related IVC cases was highest in younger women for any histological subtype. SCC with warty or basaloid features (SCC_WB) (N=326) were more likely to be HPV and p16(INK4a) positive (AP=69.5%, CI=63.6-74.8) versus KSCC (AP=11.5%, CI=9.7-13.5). HPV 16 was the commonest type (72.5%) followed by HPV 33 (6.5%) and HPV 18 (4.6%). Enrichment from VIN to IVC was significantly high for HPV 45 (8.5-fold). CONCLUSION: Combined data from HPV-DNA and p16(INK4a) testing are likely to represent a closer estimate of the real fraction of IVC induced by HPV. Our results indicate that HPV contribution in invasive vulvar cancer has probably been overestimated. HPV 16 remains the major player worldwide.
BACKGROUND:Human papillomavirus (HPV) contribution in vulvar intraepithelial lesions (VIN) and invasive vulvar cancer (IVC) is not clearly established. This study provides novel data on HPV markers in a large series of VIN and IVC lesions. METHODS: Histologically confirmed VIN and IVC from 39 countries were assembled at the Catalan Institute of Oncology (ICO). HPV-DNA detection was done by polymerase chain reaction using SPF-10 broad-spectrum primers and genotyping by reverse hybridisation line probe assay (LiPA25) (version 1). IVC cases were tested for p16(INK4a) by immunohistochemistry (CINtec histology kit, ROCHE). An IVC was considered HPV driven if both HPV-DNA and p16(INK4a) overexpression were observed simultaneously. Data analyses included algorithms allocating multiple infections to calculate type-specific contribution and logistic regression models to estimate adjusted prevalence (AP) and its 95% confidence intervals (CI). RESULTS: Of 2296 cases, 587 were VIN and 1709 IVC. HPV-DNA was detected in 86.7% and 28.6% of the cases respectively. Amongst IVC cases, 25.1% were both HPV-DNA and p16(INK4a) positive. IVC cases were largely keratinising squamous cell carcinoma (KSCC) (N=1234). Overall prevalence of HPV related IVC cases was highest in younger women for any histological subtype. SCC with warty or basaloid features (SCC_WB) (N=326) were more likely to be HPV and p16(INK4a) positive (AP=69.5%, CI=63.6-74.8) versus KSCC (AP=11.5%, CI=9.7-13.5). HPV 16 was the commonest type (72.5%) followed by HPV 33 (6.5%) and HPV 18 (4.6%). Enrichment from VIN to IVC was significantly high for HPV 45 (8.5-fold). CONCLUSION: Combined data from HPV-DNA and p16(INK4a) testing are likely to represent a closer estimate of the real fraction of IVC induced by HPV. Our results indicate that HPV contribution in invasive vulvar cancer has probably been overestimated. HPV 16 remains the major player worldwide.
Authors: David A Siegel; Reda Wilson; Edward J Wilkinson; Julia W Gargano; Meg Watson; Brenda Y Hernandez; Marc T Goodman; Charles F Lynch; Elizabeth R Unger; Mona Saraiya Journal: Arch Pathol Lab Med Date: 2016-10-20 Impact factor: 5.534
Authors: Paula Gonzalez; Allan Hildesheim; Rolando Herrero; Hormuzd Katki; Sholom Wacholder; Carolina Porras; Mahboobeh Safaeian; Silvia Jimenez; Teresa M Darragh; Bernal Cortes; Brian Befano; Mark Schiffman; Loreto Carvajal; Joel Palefsky; John Schiller; Rebeca Ocampo; John Schussler; Douglas Lowy; Diego Guillen; Mark H Stoler; Wim Quint; Jorge Morales; Carlos Avila; Ana Cecilia Rodriguez; Aimée R Kreimer Journal: Vaccine Date: 2015-03-18 Impact factor: 3.641
Authors: Laia Alemany; Maëlle Saunier; Isabel Alvarado-Cabrero; Beatriz Quirós; Jorge Salmeron; Hai-Rim Shin; Edyta C Pirog; Núria Guimerà; Gustavo Hernandez-Suarez; Ana Felix; Omar Clavero; Belen Lloveras; Elena Kasamatsu; Marc T Goodman; Brenda Y Hernandez; Jan Laco; Leopoldo Tinoco; Daan T Geraets; Charles F Lynch; Vaclav Mandys; Mario Poljak; Robert Jach; Josep Verge; Christine Clavel; Cathy Ndiaye; JoEllen Klaustermeier; Antonio Cubilla; Xavier Castellsagué; Ignacio G Bravo; Michael Pawlita; William G Quint; Nubia Muñoz; Francesc X Bosch; Silvia de Sanjosé Journal: Int J Cancer Date: 2014-05-30 Impact factor: 7.396
Authors: F Xavier Bosch; Claudia Robles; Mireia Díaz; Marc Arbyn; Iacopo Baussano; Christine Clavel; Guglielmo Ronco; Joakim Dillner; Matti Lehtinen; Karl-Ulrich Petry; Mario Poljak; Susanne K Kjaer; Chris J L M Meijer; Suzanne M Garland; Jorge Salmerón; Xavier Castellsagué; Laia Bruni; Silvia de Sanjosé; Jack Cuzick Journal: Nat Rev Clin Oncol Date: 2015-09-01 Impact factor: 66.675