Li T, Lu Z M, Chen K N, Guo M, Xing H P, Mei Q, Yang H H, Lechner J F, Ke Y
Laboratory of Genetics, Beijing Institute for Cancer Research, School of Oncology, Peking University, No. 1 Da Hong Luo Chang St, Beijing 100034, China.
Carcinogenesis. 2001 Jun;22(6):929-34. doi: 10.1093/carcin/22.6.929.
To investigate the potential role of human papillomavirus (HPV) infection in the pathogenesis of esophageal carcinomas in the Anyang area of China, we have evaluated specimens collected by balloon cytology examination from volunteers in two regions with significantly different incidences of esophageal carcinoma. 138 donors were from a village in a county with an esophageal carcinoma (EC) age-adjusted mortality rate of 132x10(5), the remaining 68 were resident in a second village from another county with an EC mortality rate of 52x10(5). Specimens were evaluated using both polymerase chain reaction (PCR) amplification and in situ hybridization (ISH) protocols. PCR results showed that the prevalence of the human papillomavirus type 16 (HPV-16) E6 gene in the high incidence area was 1.9-fold higher than that of the low incidence area (72 and 37%, respectively, P < 0.01). Moreover, the positive rate corresponded with pathology grade. Similar results were obtained with the HPV-16 E7 gene. As the cells undergoing cytopathological progress, the HPV-16 E6 positive rate was increased, in both villages. In contrast to HPV-16 E6 and E7, detection of the HPV L1 gene was consistently lower, and its prevalence decreased with increasing dysplasia grades (P < 0.05). By ISH analyses, the expression rate of HPV-16 E6 in the specimens collected from the high incidence area was 2.2-fold higher than those from the low incidence area (49 versus 22%, respectively; P < 0.05), and transcription of the E6 gene paralleled cytopathology. HPV-18 was also detected in 17 and 15% of the specimens from the high and low incidence areas, respectively, but most of these samples were also simultaneously HVP-16 positive. These results suggest that HVP-16 plays a causative role in the high incidence of esophageal cancer in the Anyang region of CHINA:
为研究人乳头瘤病毒(HPV)感染在中国安阳地区食管癌发病机制中的潜在作用,我们评估了通过气囊细胞学检查从食管癌发病率显著不同的两个地区的志愿者收集的标本。138名捐赠者来自一个县的一个村庄,该村庄食管癌(EC)年龄调整死亡率为132×10⁻⁵,其余68名居住在另一个县的第二个村庄,EC死亡率为52×10⁻⁵。使用聚合酶链反应(PCR)扩增和原位杂交(ISH)方案对标本进行评估。PCR结果显示,16型人乳头瘤病毒(HPV-16)E6基因在高发病区的流行率比低发病区高1.9倍(分别为72%和37%,P<0.01)。此外,阳性率与病理分级相对应。HPV-16 E7基因也得到了类似结果。在两个村庄中,随着细胞病理学进展,HPV-16 E6阳性率均升高。与HPV-16 E6和E7相反,HPV L1基因的检测率一直较低,其流行率随发育异常分级增加而降低(P<0.05)。通过ISH分析,从高发病区收集的标本中HPV-16 E6的表达率比低发病区高2.2倍(分别为49%和22%;P<0.05),E6基因的转录与细胞病理学平行。在高发病区和低发病区的标本中分别有17%和15%检测到HPV-18,但这些样本中的大多数同时也是HPV-16阳性。这些结果表明,HPV-16在中国安阳地区食管癌高发中起致病作用。