Worldwide human papillomavirus genotype attribution in over 2000 cases of intraepithelial and invasive lesions of the vulva.
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
de Sanjosé Silvia, Alemany Laia, Ordi Jaume, Tous Sara, Alejo Maria, Bigby Susan M, Joura Elmar Armin, Maldonado Paula, Laco Jan, Bravo Ignacio G, Vidal August, Guimerà Núria, Cross Paul, Wain Gerard V, Petry Karl Ulrich, Mariani Luciano, Bergeron Christine, Mandys Václav, Sica Adela Rosa, Félix Ana, Usubutun Alp, Seoud Muhieddine, Hernández-Suárez Gustavo, Nowakowski Andrzej Marcin, Wilson Godfrey, Dalstein Veronique, Hampl Monika, Kasamatsu Elena Sachiko, Lombardi Luis Estuardo, Tinoco Leopoldo, Alvarado-Cabrero Isabel, Perrotta Myriam, Bhatla Neerja, Agorastos Theodoros, Lynch Charles F, Goodman Marc T, Shin Hai-Rim, Viarheichyk Halina, Jach Robert, Cruz M O L Eugenia, Velasco Julio, Molina Carla, Bornstein Jacob, Ferrera Annabelle, Domingo Efren Javier, Chou Cheng-Yang, Banjo Adekunbiola F, Castellsagué Xavier, Pawlita Michael, Lloveras Belén, Quint Wim G V, Muñoz Nubia, Bosch F Xavier, HPV VVAP study group
Аннотация
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.