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In order to identify good animal models for investigating therapeutic and preventive strategies for pancreatic cancer, we analyzed pancreatic lesions from several transgenic models and made a series of novel findings. Female MT- tgf α mice of the MT100 line developed pancreatic proliferation, acinar-ductal metaplasia, multilocular cystic neoplasms, ductal adenocarcinomas and prominent fibrosis, while the lesions in males were less severe. MT- tgf α-ES transgenic lines of both sexes developed slowly progressing lesions that were similar to what was seen in MT100 males. In both MT100 and MT- tgf α-ES lines, TGFα transgene was expressed mainly in proliferating ductal cells. Ela- myc  transgenic mice with a mixed C57BL/6, SJL and FVB genetic background developed pancreatic tumors at 2–7 months of age, and half of the tumors were ductal adenocarcinomas, similar to what was reported originally by Sandgren  et al  [ 1 ]. However, in 20% of the mice, the tumors metastasized to the liver. MT100/Ela- myc  and MT- tgf α-ES/Ela- myc  double transgenic mice developed not only acinar carcinomas and mixed carcinomas as previously reported but also various ductal-originated lesions, including multilocular cystic neoplasms and ductal adenocarcinomas. The double transgenic tumors were more malignant and metastasized to the liver at a higher frequency (33%) compared with the Ela- myc  tumors. Sequencing of the coding region of  p16ink4 , k- ras  and  Rb  cDNA in small numbers of pancreatic tumors did not identify mutations. The short latency for tumor development, the variety of tumor morphology and the liver metastases seen in Ela- myc  and MT- tgf α/Ela- myc  mice make these animals good models for investigating new therapeutic and preventive strategies for pancreatic cancer.

Characterization of pancreatic lesions from MT-tgf alpha, Ela-myc and MT-tgf alpha/Ela-myc single and double transgenic mice.