AIM: To establish a gastric cancer nude-mouse model with improved orthotopic implantation and investigate its biological characteristics at different time points. METHODS: Human gastric cancer SGC-7901 cell suspensions were injected subcutaneously into a nude mouse to develop solid tumors, and the tumor tissue pieces were implanted under the serous coat. The nude mice were then euthanized in group every two weeks to observe the primary tumor growth and metastases. RESULTS: Within 2-4 wk, there were no obvious changes about the primary tumor in stomach. At the sixth week, the primary tumor began to grow fast, resulting in incrassation of the gastric wall and stenosis of the gastric cavity, and metastases into the liver and lymph nodes were detected. The tumor, which compressed the adjacent organs, gradually became bigger and bigger followed by stenosis or vanishment of the gastric cavity from 8 to 12 wk. There were massive metastases, and the rate of metastasis was 58% in lymph nodes, 78% in liver, 39% in kidney, and 81% in peritoneum or septum. CONCLUSION: A gastric cancer model is established, which can simulate the clinical tumor behavior and provide experimental carrier for clinical trials of gastric cancer treatment.
AIM: To establish a gastric cancer nude-mouse model with improved orthotopic implantation and investigate its biological characteristics at different time points. METHODS:Humangastric cancer SGC-7901 cell suspensions were injected subcutaneously into a nude mouse to develop solid tumors, and the tumor tissue pieces were implanted under the serous coat. The nude mice were then euthanized in group every two weeks to observe the primary tumor growth and metastases. RESULTS: Within 2-4 wk, there were no obvious changes about the primary tumor in stomach. At the sixth week, the primary tumor began to grow fast, resulting in incrassation of the gastric wall and stenosis of the gastric cavity, and metastases into the liver and lymph nodes were detected. The tumor, which compressed the adjacent organs, gradually became bigger and bigger followed by stenosis or vanishment of the gastric cavity from 8 to 12 wk. There were massive metastases, and the rate of metastasis was 58% in lymph nodes, 78% in liver, 39% in kidney, and 81% in peritoneum or septum. CONCLUSION: A gastric cancer model is established, which can simulate the clinical tumor behavior and provide experimental carrier for clinical trials of gastric cancer treatment.
Authors: F Maruta; A Sugiyama; K Ishida; T Ikeno; M Murakami; S Kawasaki; H Ota; M Tatematsu; T Katsuyama Journal: Cancer Lett Date: 2000-11-10 Impact factor: 8.679
Authors: T Tsuzuki; A Egashira; H Igarashi; T Iwakuma; Y Nakatsuru; Y Tominaga; H Kawate; K Nakao; K Nakamura; F Ide; S Kura; Y Nakabeppu; M Katsuki; T Ishikawa; M Sekiguchi Journal: Proc Natl Acad Sci U S A Date: 2001-09-25 Impact factor: 11.205