Abstract Background: The gastrointestinal peptide gastrin has been identified in fetal pancreas up until week 14 where it is thought to play a role in growth and differentiation. Gastrin has also been identified as an important growth factor that stimulates pancreatic cancer through the CCK-B and CCK-C receptors by an autocrine mechanism. Hypothesis: It is hypothesized that gastrin re-expression is important to pancreatic carcinogenesis. Methods: The mRNA from normal human pancreas tissue was isolated and endpoint RT-PCR was performed to detect RNA levels of gastrin and CCK peptide, using gastrin specific and CCK peptide specific primers, respectively. PCR products were visualized on an ethidium bromide stained gel after electrophoresis. Normal human pancreatic tissue samples were evaluated for gastrin and CCK by immunohistochemistry. Tissues were flash frozen and sectioned at a thickness of 8-10uM. Non-specific sites were blocked, followed by exposure to either gastrin or CCK antisera. Peptide presence was assessed using AF568 (Alexa Fluor) goat anti-rabbit secondary antibody. Results: The end-point RT-PCR showed significant levels of CCK-B receptor and CCK peptide in normal pancreas samples. The gastrin end-point RT-PCR showed extremely low levels in all of the normal pancreas samples. Gastrin immunoreactivity was not detected in normal pancreas, however, staining of the positive control, an islet cell tumor, was reactive. The negative control, a GIST tumor, showed no staining as well. Conclusions: Normal pancreas possesses the receptor CCK-B and the peptide CCK. Gastrin is not present in normal pancreatic tissues, but is detected in neoplastic pancreatic samples. Therefore, the re-expression of gastrin plays a pivotal role in the development of pancreatic cancer and could be a potential trigger to pancreatic carcinogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1110. doi:10.1158/1538-7445.AM2011-1110