Jin Jinji, Hu Changyuan, Wang Pengfei, Chen Jing, Wu Tiantian, Chen Wenjing, Ye Lulu, Zhu Guangbao, Zhang Lifang, Xue Xiangyang, Shen Xian
Department of General Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Department of Rheumatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Oncol Lett. 2014 Aug;8(2):898-904. doi: 10.3892/ol.2014.2148. Epub 2014 May 16.
The worldwide contagion, human cytomegalovirus (HCMV), may cause a series of disorders in infected individuals. The aim of the present study was to investigate whether HCMV infection is associated with the development of gastric cancer. In this study, the positive expression of unique long (UL)133-UL138 and immediate-early (IE)1 genes, which are associated with viral latency and replication, respectively, were detected using nested polymerase chain reaction. A χ test and logistic regression analysis were performed to further investigate the preliminary data. The data indicated that the positive rate of UL133, UL135 and UL136 expression in cancer tissues was higher than that in paired normal tissues (P=0.01, 0.027 and 0.013, respectively). However, no significant differences were identified in the UL133-138 locus and IE1 gene when associated with clinicopathological features. Furthermore, seven infection patterns were identified, with the UL133 + UL138 infection pattern representing the largest proportion in the cancer (60.34%) and normal tissues (42.11%). In conclusion, it is possible that the UL133-UL138 locus is important in the occurrence of gastric cancer. The mechanism by which UL133-UL138 locus expression differs in human gastric cancer requires further investigation.
全球传播的人类巨细胞病毒(HCMV)可在受感染个体中引发一系列病症。本研究的目的是调查HCMV感染是否与胃癌的发生有关。在本研究中,分别使用巢式聚合酶链反应检测与病毒潜伏和复制相关的独特长片段(UL)133 - UL138和立即早期(IE)1基因的阳性表达。进行χ检验和逻辑回归分析以进一步研究初步数据。数据表明,癌组织中UL133、UL135和UL136表达的阳性率高于配对的正常组织(分别为P = 0.01、0.027和0.013)。然而,在与临床病理特征相关时,UL133 - 138基因座和IE1基因未发现显著差异。此外,确定了七种感染模式,其中UL133 + UL138感染模式在癌组织(60.34%)和正常组织(42.11%)中占比最大。总之,UL133 - UL138基因座可能在胃癌发生中起重要作用。UL133 - UL138基因座在人类胃癌中表达差异的机制需要进一步研究。