Abstract
To establish a pancreatic cancer model in mice, dimethylbenzanthracene (DMBA) was injected into mice pancreata. By 3 months after DMBA injection into the pancreas, 6 of 10 mice showed visually recognizable tumors with precursor lesions of various types of cell atypia. The expression profiles of smad 4, cyclin D1 and p53 in the DMBA-induced tumors were similar to those of human pancreatic cancer, suggesting that this would be a useful mouse model for studying the morphologic and molecular mechanisms involved in pancreatic carcinogenesis. Semi-quantitative reverse transcription-polymerase chain reaction with microdissection demonstrated that Notch1 expression was continuous from precursor lesions to carcinoma cells compared to precursor lesions. However, no mutations of K-ras gene were detected in precancerous or cancerous lesions. Therefore, a DMBA model may be useful for understanding the mechanism underlying the transition from precursor lesions to carcinoma since such a model can show this progression without K-ras activation.
