Brief Article
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World J Gastroenterol. Dec 28, 2011; 17(48): 5295-5304
Published online Dec 28, 2011. doi: 10.3748/wjg.v17.i48.5295
Human papillomavirus in upper digestive tract tumors from three countries
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
Andres Castillo, Chihaya Koriyama, Muhammad Anwar, Suminori Akiba, Department of Epidemiology and Preventive Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan
Michiyo Higashi, Department of Human Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan
Mulazim Hussain Bukhari, King Edward Medical University, Lahole 54000, Pakistan
Edwin Carrascal, Department of Pathology, Universidad del Valle, Cali 760043, Colombia
Lida Mancilla, Universidad Santiago de Cali, Cali 760035, Colombia
Hiroshi Okumura, Masataka Matsumoto, Shoji Natsugoe, Department of Surgical Oncology and Digestive Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan
Kazumasa Sugihara, Department of Maxillofacial Diagnostic and Surgical Science, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan
Yoshito Eizuru, Division of Oncogenic and Persistent Viruses, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan
Author contributions: Castillo A, Koriyama C and Akiba S conceived the study, analyzed the data and participated in editing of the manuscript; Castillo A performed human papillomavirus analysis; Higashi M, Bukhari MH and Carrascal E conducted pathological analyses; Anwar M, Mancilla L, Okumura H, Matsumoto M, Sugihara K and Natsugoe S retrieved clinical information and obtained a collection of tissue specimens for analysis; Eizuru Y and Akiba S gave analytical support for all the analyses.
Supported by Grants-in-Aid for Scientific Research on Priority Areas (17015037) of the Ministry of Education, Culture, Sports, Science and Technology, Japan
Correspondence to: Dr. Chihaya Koriyama, Department of Epidemiology and Preventive Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8544,Japan. fiy@m.kufm.kagoshima-u.ac.jp
Telephone: +81-99-2755298 Fax: +81-99-2755299
Received: April 21, 2011
Revised: July 11, 2011
Accepted: July 18, 2011
Published online: December 28, 2011
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.

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