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Human papillomavirus in upper digestive tract tumors from three countries

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Author(s): Andres Castillo | Chihaya Koriyama | Michiyo Higashi | Muhammad Anwar | Mulazim Hussain Bukhari | Edwin Carrascal | Lida Mancilla | Hiroshi Okumura | Masataka Matsumoto | Kazumasa Sugihara | Shoji Natsugoe | Yoshito Eizuru | Suminori Akiba

Journal: World Journal of Gastroenterology
ISSN 1007-9327

Volume: 17;
Issue: 48;
Start page: 5295;
Date: 2011;
Original page

Keywords: Human papillomavirus | Viral load | Physical status | E6 | p53 | p16INK4a

ABSTRACT
AIM: 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.
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