Earlier Helicobacter pylori infection increases the risk for the N-methyl-N-nitrosourea-induced stomach carcinogenesis in Mongolian gerbils.

Earlier Helicobacter pylori infection increases the risk for the N-methyl-N-nitrosourea-induced stomach carcinogenesis in Mongolian gerbils.
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DOI:
10.1111/j.1349-7006.2002.tb01237.x
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发表时间:
2002-12
期刊:
Japanese journal of cancer research : Gann
影响因子:
--
通讯作者:
Tatematsu M
Tatematsu M
中科院分区:
其他
文献类型:
--
作者:
Cao X;Tsukamoto T;Nozaki K;Tanaka H;Shimizu N;Kaminishi M;Kumagai T;Tatematsu M

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幽门螺杆菌(H.幽门螺杆菌)与胃癌有关,在儿童时期而不是成年时感染被认为对致癌作用更重要。目的:探讨胃癌发生的易感性与H。pylori感染,我们设计了一个实验,包括接种H. pylori ATCC 43504,然后在不同年龄进行N-甲基-N-亚硝基脲(MNU)治疗。将4周龄雄性蒙古沙鼠(MG)分为12组。H. pylori分别在4、18和32周龄时接种,作为早期、中期和晚期感染的代表。两周后,用MNU处理动物。不含H. pylori和/或MNU作为对照。接种后52周早期(H。pylori+MNU)、中度(H. pylori+MNU)和晚期(H. pylori+MNU组为60%(12/ 20),MNU组为18.4%(2/11),MNU组为10%(2/20)。MNU单药组的相应数字分别为14.8%(4/27)、0%(0/11)和0%(0/21)。血清H. pylori感染早期组较中、晚期组高(P<0.01),胃泌素水平也较中、晚期组高(P<0.01)。结果清楚地表明,早期获得H。与后来感染的病例相比,幽门螺杆菌感染显著增加了MNU的胃化学致癌作用,这可能是由于宿主胃粘膜因子和免疫应答的差异。
Helicobacter pylori (H. pylori) is now well known to be associated with stomach cancer, with infection during childhood rather than as an adult considered to be more important for carcinogenesis. To evaluate the difference in susceptibility to stomach carcinogenesis in relation to age of acquisition of H. pylori infection, we designed an experiment involving inoculation of H. pylori ATCC43504 followed by N‐methyl‐N‐nitrosourea (MNU) treatment at different ages. Four‐week‐ old male Mongolian gerbils (MGs) were divided into twelve groups. H. pylori was inoculated at 4, 18 and 32 weeks of age, as representatives of early, middle and late infection, respectively. Two weeks later, the animals were treated with MNU. Groups without H. pylori and/or MNU were included as controls. The incidences of adenocarcinomas at 52 weeks after the inoculation in the early (H. pylori+MNU), middle (H. pylori+MNU), and late (H. pylori+MNU) group were 60% (12/ 20), 18.4% (2/11), and 10% (2/20), respectively. The corresponding figures were 14.8% (4/27), 0% (0/11), and 0% (0/21) in the MNU‐alone groups. A higher titer of serum IgG for H. pylori and higher gastrin level were seen in the early‐infected compared to the middle and the late groups (P<0.01). The results clearly demonstrated that early acquisition of H. pylori significantly increases gastric chemical carcinogenesis with MNU, as compared to the case with later infection, possibly because of differences in host gastric mucosal factors and immunologic responses.
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