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Open Access Highly Accessed Research article

Comparison of prevalence, viral load, physical status and expression of human papillomavirus-16, -18 and -58 in esophageal and cervical cancer: a case-control study

Donghong Zhang1, Qingying Zhang2, Li Zhou3, Leijun Huo1, Yi Zhang4, Zhongying Shen5 and Yi Zhu1*

Author Affiliations

1 Cardiovascular Research Center, Shantou University Medical College, 22 Xinling Road, Shantou, Guangdong, 515041, China

2 Department of Preventive Medicine, Shantou University Medical College, 22 Xinling Road, Shantou, Guangdong, 515041, China

3 Department of Gynecologic Medical Oncology, Affiliated Cancer Hospital of Shantou University Medical College, 22 Xinling Road, Shantou, Guangdong, 515041, China

4 Department of Physiology and Pathophysiology, Peking University Health Sciences Center, 38 Xueyuan Road, Beijing, 100191, China

5 Institute of Oncology Pathology, Shantou University Medical College, 22 Xinling Road, Shantou, Guangdong, 515041, China

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BMC Cancer 2010, 10:650  doi:10.1186/1471-2407-10-650

Published: 26 November 2010

Abstract

Background

Human papillomavirus (HPV) infection is a major risk factor for the development of nearly all cases of cervical cancer worldwide. The presence of HPV DNA in cases of esophageal squamous-cell carcinoma (ESCC) has been reported repeatedly from Shantou, China, and other regions with a high incidence of esophageal carcinoma (EC). However, unlike in cervical squamous-cell carcinoma (CSCC), in ESCC, the characteristics of HPV are unclear. Thus, the role of high-risk HPV types in the carcinogenesis of ESCC remains uncertain.

Methods

Seventy cases of ESCC with 60 controls and 39 cases of CSCC with 54 controls collected from patients in Shantou region in China were compared for the distributions of HPV-16, -18 and -58; viral load; and viral integration using real-time PCR assay and HPV-16 expression using immunostaining.

Results

The detection rates and viral loads of HR-HPV infection were significantly lower in ESCC than in CSCC (50.0% vs. 79.48%, P = 0.005; 2.55 ± 3.19 vs. 361.29 ± 441.75, P = 0.002, respectively). The combined integration level of HPV-16, -18 and -58 was slightly lower in ESCC than in CSCC (P = 0.022). HPV-16 expression was detected in 59.26% of ESCC tissue and significantly associated with tumour grade (P = 0.027).

Conclusions

High levels of HR-HPV expression and integration may be an indicator of the risk of ESCC, at least for patients in the Shantou region of China. However, a relatively low HPV copy number and infection rate in ESCC is unlikely to play an essential a role in the carcinogenesis of ESCC as in cervical cancer. Factors other than HR-HPV infection may contribute to the carcinogenesis of ESCC.