Two types of peritoneal dissemination of pancreatic cancer cells in a hamster model.

Peritoneal dissemination has an unfavorable impact on the prognosis of pancreatic cancer, and a peritoneal dissemination model was created in hamsters by using an experimental pancreatic cancer to clarify its pathological characteristics. PGHAM-1, a cancer cell line we established from BOP induced pancreatic cancer in Syrian golden hamsters, was inoculated into the abdominal cavity of Syrian golden hamsters. After inoculation, sequential changes in the diaphragm, omentum, and parietal peritoneum, and the metastatic patterns of the PGHAM-1 cells were morphologically investigated by macroscopical, microscopical, and ultrastructural observation. The cancer cells were easily absorbed at the stomata in the diaphragm and milky spots in the omentum, which were absorptive lymphatic structures, and lymphatic metastasis occurred 4 days after inoculation. In the parietal peritoneum, however, the cancer cells attached to and proliferated on the parietal peritoneum where mesothelial cells had exfoliated and the basement membrane was exposed. This process was comparatively time-consuming, and metastasis occurred in the parietal peritoneum at 7 days after inoculation. This study suggested that there might be two patterns of peritoneal dissemination of hamster pancreatic cancer. One route is lymphatic metastasis via stomata in the diaphragm and milky spots in the omentum, and the other is direct metastasis on the parietal peritoneum; each metastasis forms independently.