Liao Pei-hua, Qin Jiang-mei, Zeng Tong-xia, Li Feng, Cai Jin-feng, He Ling
Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University, Shihezi 832002, China.
Zhonghua Liu Xing Bing Xue Za Zhi. 2009 Sep;30(9):951-4.
To evaluate the role and the association between HPV16E6 infection and HLA-DR9 immune-associated gene to esophageal cancer (EC) in Kazakh of Xinjiang, China.
A 1:2 matched case-control study was conducted with 63 cases of EC and 126 controls involved. The controls were matched by sex, nationality, area of residence and age within 5-year difference. HPV16E6 and HLA-DR9 allele were identified by PCR-SSP. Interaction was performed to identify risk factors.
HPV16E6 infection and HLA-DR9 allele positive status were the risk factors for EC, with OR values as 2.67 (95%CI: 1.38 - 5.17) and 3.83 (95%CI: 1.48 - 9.96) respectively. The rate of HPV16E6 infection in individuals with HLA-DR9 allele was different from the ones who were HLA-DR9 allele free (chi(2) = 7.57, P = 0.006), with OR value as 5.79 (95%CI: 1.53 - 21.87). In the controls, the rates of HPV16E6 infection were 22.2% and 16.2% among individuals with HLA-DR9 allele atatus as positive or negative, and without statistically significant difference. Interaction analysis showed there was an interaction of HPV16E6 with HLA-DR9 and were higher than the sum of the two factors presented individually.
In our study, we found that the HLA-DR9 allele and HPV16E6 infection had a function of synergy in the process of malignant transformation of esophageal epithelial cells, and jointly promoting the occurrence and development of EC.
评估人乳头瘤病毒16E6(HPV16E6)感染与HLA - DR9免疫相关基因在新疆哈萨克族食管癌(EC)中的作用及关联。
开展一项1:2匹配的病例对照研究,纳入63例食管癌患者和126例对照。对照按照性别、民族、居住地区和年龄相差不超过5岁进行匹配。采用聚合酶链反应 - 序列特异性引物(PCR - SSP)法鉴定HPV16E6和HLA - DR9等位基因。进行交互作用分析以确定危险因素。
HPV16E6感染和HLA - DR9等位基因阳性状态是食管癌的危险因素,比值比(OR)值分别为2.67(95%可信区间:1.38 - 5.17)和
3.83(95%可信区间:1.48 - 9.96)。携带HLA - DR9等位基因个体的HPV16E6感染率与不携带HLA - DR9等位基因个体不同(χ² = 7.57,P = 0.006),OR值为5.79(95%可信区间:1.53 - 21.87)。在对照中,HLA
在本研究中,我们发现HLA - DR9等位基因和HPV16E6感染在食管上皮细胞恶性转化过程中具有协同作用,共同促进食管癌的发生发展。