Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Virology. 2011 Dec 20;421(2):114-8. doi: 10.1016/j.virol.2011.09.018. Epub 2011 Oct 13.
Ninety percent of anal cancer is associated with human papilloma viruses (HPVs). Using our previously established HPV transgenic mouse model for anal cancer, we tested the role of the individual oncogenes E6 and E7. K14E6 and K14E7 transgenic mice were treated with dimethylbenz[a]anthracene (DMBA) to the anal canal and compared to matched nontransgenic and doubly transgenic K14E6/E7 mice. K14E7 and K14E6/E7 transgenic mice developed anal tumors (papillomas, atypias and carcinomas combined) at significantly higher rates (88% and 100%, respectively) than either K14E6 or NTG mice (18% and 19%, respectively). Likewise, K14E7 and K14E6/E7 transgenic mice developed frank cancer (carcinomas) at significantly higher rates (85% and 85%, respectively) than either K14E6 or NTG mice (18% and 10%, respectively). These findings indicate that E7 is the more potent oncogene in anal cancer caused by HPVs.
90%的肛门癌与人类乳头瘤病毒（HPV）有关。我们使用先前建立的肛门癌 HPV 转基因小鼠模型，测试了个别致癌基因 E6 和 E7 的作用。K14E6 和 K14E7 转基因小鼠接受二甲苯并[a]蒽（DMBA）处理肛门，并与匹配的非转基因和双转基因 K14E6/E7 小鼠进行比较。K14E7 和 K14E6/E7 转基因小鼠发展肛门肿瘤（包括乳头瘤、异型增生和癌）的比例明显高于 K14E6 或 NTG 小鼠（分别为 88%和 100%，而分别为 18%和 19%）。同样，K14E7 和 K14E6/E7 转基因小鼠发展明显更高比例的肛门癌（癌），分别为 85%和 85%，而 K14E6 或 NTG 小鼠分别为 18%和 10%。这些发现表明，E7 是 HPV 引起的肛门癌中更有效的致癌基因。
