Human papillomavirus not detected in esophageal adenocarcinoma tumor specimens-Reply
| Autor: | Annika Antonsson, Lani Knight, David C. Whiteman |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
Cancer Research
Pathology medicine.medical_specialty Esophageal Neoplasms Epidemiology Population Esophageal adenocarcinoma Adenocarcinoma ORIGINAL CONTRIBUTIONS 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Humans Papillomaviridae Esophagus Human papillomavirus education Human papillomavirus 16 education.field_of_study Human papillomavirus 18 biology business.industry Papillomavirus Infections virus diseases medicine.disease biology.organism_classification medicine.anatomical_structure Oncology chemistry 030220 oncology & carcinogenesis Barrett's esophagus 030211 gastroenterology & hepatology business DNA |
| Zdroj: | Cancer Epidemiology. 43:120 |
| ISSN: | 1877-7821 |
| Popis: | Human papillomavirus (HPV) causes the majority of oropharyngeal cancers in the United States, yet the risk factors for and natural history of oral HPV infection are largely unknown. In 2010–2011, a US-based longitudinal cohort study of 761 human immunodeficiency virus (HIV)-infected and 469 at-risk HIV-uninfected participants from the Multicenter AIDS Cohort Study and the Women's Interagency HIV Study was initiated. Semiannually collected oral rinses were evaluated for 37 HPV genotypes using the Roche LINEAR ARRAY HPV Genotyping Test (Roche Molecular Systems, Pleasanton, California), and factors associated with oral HPV incidence and clearance were explored using adjusted Wei-Lin-Weissfeld modeling. Through 2013, the 2-year cumulative incidence of any type of oral HPV infection was 34% in HIV-infected persons and 19% in HIV-uninfected persons. However, many of these infections cleared. Seven percent of incident infections and 35% of prevalent infections persisted for at least 2 years. After adjustment for other risk factors, HIV infection (adjusted hazard ratio = 2.3, 95% confidence interval: 1.7, 3.2), reduced current CD4 cell count, and increased numbers of oral sex and “rimming” partners increased the risk of incident oral HPV infection, whereas male sex, older age, and current smoking increased the risk of oral HPV persistence (each P < 0.05). This helps explain the consistent associations observed between these factors and prevalent oral HPV infection in previous cross-sectional studies. |
| Databáze: | OpenAIRE |
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