Sato Takahiro, Miwa Koichi, Sahara Hiroyuki, Segawa Masataka, Hattori Takanori
Department of Second Surgery, School of Medicine Kanazawa University, Ishikawa, Japan.
Anticancer Res. 2002 Jan-Feb;22(1A):39-44.
The experiment was designed to sequentially examine the histogenesis of Barrett's esophagus and esophageal adenocarcinoma induced by duodenal reflux without exogenous carcinogens.
Wistar male rats, 200 in all, each weighing approximately 250 g were used. The totally gastrectomized animals were reconstructed by Schlatter's method to produce duodeno-esophageal reflux (n = 100), for comparison with no reflux, Roux-en-Y reconstruction (n = 100). The excised esophagus was histopathologically examined every 10 weeks after surgery until 50 weeks.
Among the animals with reflux, Barrett's epithelium developed near esophago-jejunostoma 10 weeks after surgery and subsequently spread upward. Columnar dysplasia was first identified in the zone of Barrett's epithelium at 20 weeks, simultaneously with adenocarcinoma. As the incidence of Barrett's esophagus increased over time, the incidence of both dysplasia and adenocarcinoma also increased. Adenocarcinoma developed in the area of columnar dysplasia.
The temporal progression from Barrett's esophagus to columnar dysplasia and adenocarcinoma is induced by duodeno-esophageal reflux. Columnar dysplasia is a morphological marker for adenocarcinogenesis.
本实验旨在依次研究在无外源性致癌物情况下十二指肠反流诱导的巴雷特食管和食管腺癌的组织发生过程。
总共使用200只雄性Wistar大鼠,每只体重约250克。通过施拉特方法对全胃切除的动物进行重建以产生十二指肠 - 食管反流(n = 100),与无反流的Roux - en - Y重建(n = 100)进行比较。术后每10周对切除的食管进行组织病理学检查,直至50周。
在有反流的动物中,术后10周在食管空肠吻合口附近出现巴雷特上皮,随后向上蔓延。20周时在巴雷特上皮区域首次发现柱状上皮发育异常,同时发现腺癌。随着巴雷特食管发病率随时间增加,发育异常和腺癌的发病率也增加。腺癌在柱状上皮发育异常区域发生。
十二指肠 - 食管反流可诱导从巴雷特食管到柱状上皮发育异常和腺癌的时间进程。柱状上皮发育异常是腺癌发生的形态学标志。