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Ya-Wen Wang [1] and Kai Zhang [1] and Song Zhao [1] and Yanrong Lv [1] and Jiang Zhu [1] and Huantao Liu [1] and Jinbo Feng [2] and Weili Liang [1] and Rong Ma [1] and Jianli Wang [3]

Academic Editor: Anne Hamburger

1, Department of Breast Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China, qiluhospital.com

2, Gene Laboratory, Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, Shandong, China, qiluhospital.com

3, Department of Pathophysiology, School of Medicine, Shandong University, Jinan, Shandong, China, sdu.edu.cn

Received Jun 30, 2017; Accepted Nov 19, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Recent studies have reported that some viruses such as Epstein-Barr virus (EBV) and mouse mammary tumor virus (MMTV), as well as human papillomavirus (HPV), may play important roles in breast cancer development and progression [1]. The relationship between HPV and other types of cancers, including cervix, vagina, vulva, head and neck, anal, and penile carcinomas, has been well established [2]. However, reports on the association between HPV and breast cancer were controversial. The prevalence of HPV in breast cancer tissues ranged from 0 to 86% [3]. Although a number of studies have supported the involvement of HPV in breast cancer, several other investigations did not detect any HPV subtypes in breast cancer tissues [4]. It is important to further clarify the role and mechanism of HPV in breast cancer.

HPVs are small, circular, double-stranded DNA viruses. Approximately 200 different HPVs have now been identified and these viruses can be classified into mucosal and cutaneous HPVs [5]. The mucosal HPV types are designated as “low-risk” and “high-risk” types based on the propensity for malignant progression of the lesions that they cause [5]. Low-risk HPV subtypes, such as HPV 6 and HPV 11, cause more than 90% of genital warts, whereas high-risk HPV subtypes (HPVs 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68) cause squamous intraepithelial lesions that can progress to invasive squamous cell carcinomas [4]. Cell cycle and apoptosis are critical events during cell transformation and carcinogenesis [6]. The high-risk HPV E6 and...
       
 
       
 
 
       
 
     
       
 
     
       
 
       
 
       
 
       
 
     
       
 
     
 
     
 
     
 
     
 
     
 

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