Dai Min, Clifford Gary M, le Calvez Florence, Castellsagué Xavier, Snijders Peter J F, Pawlita Michael, Herrero Rolando, Hainaut Pierre, Franceschi Silvia
IARC, Lyon, France.
Cancer Res. 2004 Jan 15;64(2):468-71. doi: 10.1158/0008-5472.can-03-3284.
TP53 mutations were analyzed in 35 human papillomavirus (HPV) type 16 DNA-positive cancers of the oral cavity and oropharynx and in 35 HPV DNA-negative cancers matched by subsite, country, sex, age, and tobacco and alcohol consumption. Wild-type TP53 was found more frequently in cancer specimens that contained HPV16 DNA than in those that did not. All 14 HPV16 DNA-positive cancers in HPV16 E6 antibody-positive patients contained wild-type TP53, compared with 50% of corresponding HPV DNA-negative cancers (matched odds ratio, infinity; 95% confidence interval, 1.4- infinity ). In contrast, for HPV16 DNA-positive cancers in E6-negative patients, wild-type TP53 frequency was similar to that in corresponding HPV DNA-negative cancers (matched odds ratio, 1.0; 95% confidence interval, 0.2-5.4). TP53 inactivation is a major mechanism of HPV-related carcinogenesis in the oral cavity and oropharynx. The role of HPV in cancers also containing TP53 mutations remains to be clarified.
对35例口腔和口咽的人乳头瘤病毒16型（HPV-16）DNA阳性癌症以及35例按亚部位、国家、性别、年龄、烟草和酒精消耗量匹配的HPV DNA阴性癌症进行了TP53突变分析。在含有HPV16 DNA的癌症标本中，野生型TP53比在不含有该病毒的标本中更常见。在HPV16 E6抗体阳性患者的所有14例HPV16 DNA阳性癌症中，均含有野生型TP53，而相应的HPV DNA阴性癌症中这一比例为50%（匹配优势比，无穷大；95%置信区间，1.4至无穷大）。相比之下，在E6阴性患者的HPV16 DNA阳性癌症中，野生型TP53的频率与相应的HPV DNA阴性癌症相似（匹配优势比，1.0；95%置信区间，0.2至5.4.4）。TP53失活是口腔和口咽中HPV相关致癌作用的主要机制。HPV在也含有TP53突变的癌症中的作用仍有待阐明。
