Human papillomavirus in upper digestive tract tumors from three countries

dc.contributor.authorCastillo, Andrés
dc.contributor.authorKoriyama, Chihaya
dc.contributor.authorHigashi, Michiyo
dc.contributor.authorAnwar, Muhammad Maqsood
dc.contributor.authorBukhari, Mulazim Hussain
dc.contributor.authorCarrascal, Edwin
dc.contributor.authorMancilla, Lida I.
dc.contributor.authorMatsumoto, Matsutaka
dc.contributor.authorSugihara, Kazumasa
dc.contributor.authorNatsugoe, Shoji
dc.contributor.authorEizuru, Yoshito
dc.contributor.authorAkiba, Suminori
dc.contributor.authorOkumura, Hiroshi
dc.date.accessioned2019-07-10T19:44:03Z
dc.date.available2019-07-10T19:44:03Z
dc.date.issued2011-12-28
dc.description.abstractAIM: To clarify human papillomavirus (HPV) involvement in carcinogenesis of the upper digestive tract of virological and pathological analyses. METHODS: The present study examined the presence of HPV in squamous cell carcinomas of the oral cavity (n = 71), and esophagus (n = 166) collected from Japan, Pakistan and Colombia, with different HPV exposure risk and genetic backgrounds. The viral load and physical status of HPV16 and HPV16-E6 variants were examined. Comparison of p53 and p16INK4a expression in HPV-positive and HPV-negative cases was also made. RESULTS: HPV16 was found in 39 (55%) oral carcinomas (OCs) and 24 (14%) esophageal carcinomas (ECs). This site-specific difference in HPV detection between OCs and ECs was statistically significant (P < 0.001). There was a significant difference in the geographical distribution of HPV16-E6 variants. Multiple infections of different HPV types were found in 13 ECs, but multiple infections were not found in OCs. This difference was statistically significant (P = 0.001). The geometric means (95% confidence interval) of HPV16 viral load in OCs and ECs were 0.06 (0.02-0.18) and 0.12 (0.05-0.27) copies per cell, respectively. The expression of p16INK4a proteins was increased by the presence of HPV in ECs (53% and 33% in HPV-positive and -negative ECs, respectively; P = 0.036), and the high-risk type of the HPV genome was not detected in surrounding normal esophageal mucosa of HPV-positive ECs. CONCLUSION: Based on our results, we cannot deny the possibility of HPV16 involvement in the carcinogenesis of the esophagus. © 2011 Baishideng. All rights reserved.en_US
dc.identifier.issn10079327
dc.identifier.urihttps://repositorio.usc.edu.co/handle/20.500.12421/357
dc.language.isoenen_US
dc.subjectE6en_US
dc.subjectHuman papillomavirusen_US
dc.subjectp16INK4aen_US
dc.subjectP53en_US
dc.subjectPhysical statusen_US
dc.subjectViral loaden_US
dc.subjectProtein p16en_US
dc.subjectProtein p53en_US
dc.subjectDigestive system canceren_US
dc.subjectEsophagus carcinomaen_US
dc.subjectHuman tissueen_US
dc.subjectNonhumanen_US
dc.subjectCarcinoma, Squamous Cellen_US
dc.subjectAgeden_US
dc.subjectCell Transformation, Neoplasticen_US
dc.subjectMiddle Ageden_US
dc.subjectColombiaen_US
dc.subjectJapanen_US
dc.subjectPakistanen_US
dc.subjectOncogene Proteins, Viralen_US
dc.titleHuman papillomavirus in upper digestive tract tumors from three countriesen_US
dc.typeArticleen_US

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