Takenaka Yoshiharu, Tsukamoto Tetsuya, Mizoshita Tsutomu, Cao Xueyuan, Ban Hisayo, Ogasawara Naotaka, Kaminishi Michio, Tatematsu Masae
Division of Oncological Pathology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa, Nagoya, Japan.
Cancer Sci. 2006 Oct;97(10):1015-22. doi: 10.1111/j.1349-7006.2006.00273.x.
Intestinal metaplasia has been investigated extensively as a possible premalignant condition for stomach cancer but its pathogenesis is still not fully understood. In the present study, we examined the relationship between endocrine and mucous cell marker expression periodically after Helicobacter pylori infection in the Mongolian gerbil model. The numbers of chromogranin A (CgA)-positive, gastrin-positive and gastric inhibitory polypeptide (GIP)-positive cells in H. pylori-infected groups was increased significantly compared with the non-infected case. However, CgA-positive and gastrin-positive cells then decreased from 50 through 100 experimental weeks after H. pylori infection, whereas GIP-positive cells increased. Coexistence of gastrin-positive and GIP-positive cells was detected in the same gastric and intestinal mixed phenotypic glandular-type glands. In conclusion, the endocrine cell phenotype is in line with that of the mucous counterpart in the glands of H. pylori-infected Mongolian gerbil stomach, supporting the concept that development of intestinal metaplasia is due to the abnormal differentiation of a stem cell.
肠化生作为胃癌可能的癌前病变已得到广泛研究，但其发病机制仍未完全阐明。在本研究中，我们在蒙古沙鼠模型中，于幽门螺杆菌感染后定期检测内分泌细胞和黏液细胞标志物表达之间的关系。与未感染组相比，幽门螺杆菌感染组中嗜铬粒蛋白A（CgA）阳性、胃泌素阳性和胃抑制多肽（GIP）阳性细胞数量显著增加。然而，幽门螺杆菌感染后50至100个实验周，CgA阳性和胃泌素阳性细胞数量减少，而GIP阳性细胞数量增加。在相同的胃和肠混合表型腺型腺体中检测到胃泌素阳性和GIP阳性细胞共存。总之，幽门螺杆菌感染的蒙古沙鼠胃腺体中，内分泌细胞表型与黏液细胞表型一致，支持肠化生的发生是由于干细胞异常分化这一观点。
