中文摘要：

调查 N 的增加的效果的目的，在在 TgN (p53mt-LMP1 )/HT 之中的鼻音或鼻咽的 epithelia 的导致的 carcinogenesis 上的 N′-dinitrosopiperazine (DNP ) 为鼻咽的癌(NPC ) 的发展检验内在的机制的转基因的老鼠。转基因的老鼠和一样 C ₅₇分别地， BL/6J 野类型的老鼠随机两个都在平行在 5 个月岁时被划分成 2 个组即， TgN ( p53mt-LMP1 ) /HT 癌的导致损害的组( TI )， TgN ( p53mt-LMP1 ) /HT 控制组( TC )， C ₅₇ BL/6J 癌的导致损害的组( CI )，和 C ₅₇ BL/6J 控制组( CC )。TI 和 CI 鼠标仅仅与 DNP 被对待 16 个星期，两次每个星期，当 TC 和 CC 鼠标被给一样的卷时象控制盐。在处理的结束，动物被牺牲由 haematoxylin 和曙红为 pathohistological 评估从鼻音洞和鼻咽收集上皮的织物样品(他) 染色并且为由免疫组织化学的 TRAF2， c6 月，和 p16 的表示上的决心。结果不正常的增生比在 TC ， CI ，和 CC 的那些在 TI 的样品是更重要的，与是的损害的率90%，10%， 0 ，和 0 ( P【0.01 )分别地，不过， DNP 象往常一样在更少的剂量并且没有 carcinogenic 倡导者 12-O-tetradecanoylphorbol-13-acetate 的使用在一个很弄短的导致的时期独自被使用。肿瘤坏死因素(TNF ) 的表情联系受体的因素 2 (TRAF2 ) 并且在这些样品的 c6 月在 TI (P【0.01 ) 是显著地起来调整的，当 p16 的表示比在另外的组(P【0.01 ) 在 TI 是显著地更低的时。结论 TgN (p53mt-LMP1 )/HT 鼠标保持在有免疫力的监视功能继承了宪政的缺点，它能被环境致癌物加重，例如使用的 DNP 尽管在少得多力量。TgN (p53mt-LMP1 )/HT 老鼠上的 DNP 的提高的导致 carcinogenesis 效果应该仔细与使活跃之物 protein-1 (AP-1 ) 的反常发信号被联系小径， TRAF2 和 c6 月的特别起来调整的表情，和 p16 的下面调整的表示。

英文摘要：

Objective： To investigate the enhancive effect ofN, N′-dinitrosopiperazine （DNP） on induced carcinogenesis in nasal and/or nasopharyngeal epithelia among TgN（p53mt-LMP1）/HT transgenic mice to examine the underlying mechanism for the development of nasopharyngeal carcinoma （NPC）. Methods： TgN（p53mt-LMP1）/HT transgenic mice and the same strain of C57BL/6J wild-type mice both at the age of 5 months were randomly divided into 2 groups in parallel, respectively, i.e., TgN（p53mt-LMP1）/HT cancerous lesion-inducing group （T1）, TgN（p53mt-LMP1）/HT control group （TC）, C57BL/6J cancerous lesion-inducing group （CI）, and C57BL/6J control group （CC）. TI and CI mice were treated only with DNP for 16 weeks, twice each week, while TC and CC mice were given the same volume of saline as controls.At the end of treatment, animals were sacrificed to collect epithelial tissue samples from nasal cavity and nasopharynx for pathohistological evaluation by hacmatoxylin and eosin （HE） staining and for determination on the expression ofTRAF2, c-Jun, and p 16 by immunohistochemistry. Results： Atypical hyperplasia was more significant in the samples of TI than in those of TC, CI, and CC, with the rates of lesions being 90%, 10%, 0, and 0 （P〈0.01） respectively, though DNP was used alone in a much shortened inducing period at less dosage and without the use of carcinogenic promoter 12-0-tetradecanoylphorbol-13-acetate as usual. The expressions of tumor necrosis factor （TNF） receptor-associated factor 2 （TRAF2） and c-Jun in these samples were significantly up-regulated in TI （P〈0.0 I）, while tbe expression of p16 was significantly lower in TI than in the other groups （P〈0.01）. Conclusion： TgN（p53mt-LMPI）/HT mice hold inherited constitutional defect in immune surveillance function, which can be aggravated by environmental carcinogens, such as DNP used even though in a much less strength. The enhanced carcinogenesis-inducing effect of DNP on TgN（p53mt-LMP1）/HT mi