Li Shuying, Shen Haie, Li Ji, Hou Xiaoli, Zhang Ke, Li Jintao
Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, North China University of Science and Technology, Tangshan, China.
College of Life Science and Bio-engineering, Beijing University of Technology, Beijing, China.
Turk J Gastroenterol. 2018 Mar;29(2):157-163. doi: 10.5152/tjg.2018.17568.
BACKGROUND/AIMS: To investigate the etiology of esophageal cancer (EC) related with human papillomavirus (HPV) infection.
Fresh surgically resected tissue samples and clinical information were obtained from 189 patients. Genomic DNA was extracted, and HPV was detected using polymerase chain reaction (PCR) with HPV L1 gene primers of MY09/11; HPV16 was detected using HPV16 E6 type-specific primer sets. Copies of HPV16 E2, E6, and the human housekeeping gene β-actin were tested using quantitative PCR to analyze the relationship between HPV16 integration and esophageal squamous cell carcinoma and the relationship between the HPV16 integration status and clinical information of patients.
Of the 189 samples, 168 HPV-positive samples were detected, of which 76 were HPV16 positive. Among the HPV16 positive samples, 2 cases (E2/E6 ratio>1) were 2.6% (2/76) purely episomal, 65 (E2/E6 ratio between 0 and 1) were 85.6% (65/76) mixture of integrated and episomal, and 9 (E2/E6 ratio=0) were 11.8% (9/76) purely integrated. The results indicate that integration of HPV16 was more common in the host genome than in the episome genome. The prevalence rate of HPV16 integration is increasing with the pathological stage progression of esophageal carcinoma (EC).
A high prevalence of HPV16 suggested that HPV16 has an etiological effect on the progress of EC. Integration of HPV16 is more common than episome genome in the host cells, indicating that continuous HPV infection is the key to esophageal epithelial cell malignant conversion and canceration.
背景/目的：探讨与人乳头瘤病毒（HPV）感染相关的食管癌（EC）病因。
获取189例患者手术切除的新鲜组织样本及临床信息。提取基因组DNA，使用针对HPV L1基因的MY09/11引物通过聚合酶链反应（PCR）检测HPV；使用HPV16 E6型特异性引物组检测HPV16。采用定量PCR检测HPV16 E2、E6及人类管家基因β-肌动蛋白的拷贝数，以分析HPV16整合与食管鳞状细胞癌的关系以及HPV16整合状态与患者临床信息的关系。
189份样本中，检测到168份HPV阳性样本，其中76份为HPV16阳性。在HPV16阳性样本中，2例（E2/E6比值>1）为2.6%（2/76）纯游离型，65例（E2/E6比值在0至1之间）为85.6%（65/76）整合型与游离型混合，9例（E2/E6比值=0）为11.8%（9/76）纯整合型。结果表明，HPV16在宿主基因组中的整合比在游离基因组中更常见。HPV16整合的发生率随食管癌（EC）病理分期进展而增加。
HPV16的高流行率表明HPV16在EC进展中具有病因学作用。HPV16在宿主细胞中的整合比游离基因组更常见，表明持续的HPV感染是食管上皮细胞恶性转化和癌变的关键。
