Purpose: Pancreatic cysts, which could represent malignant, pre-malignant, or benign lesions, are being detected more frequently due to improvements in imaging techniques. Although the natural history of cysts is not fully understood, accurate characterization of cysts is paramount to optimize patient care. Cyst fluid cytology, CEA marker, and more recently, K-ras gene analysis, have all been used in an attempt to characterize cysts. In this study, we undertook an analysis of our experience at UMMHC over the past seven years with different methods of predicting pancreatic cyst type, focusing specifically on the utility of K-ras gene analysis in improving clinical decision making. Methods: We requested the medical record numbers of all patients seen at UMMHC over the last seven years who were coded with ICD-9 code 577.2, which represents the diagnosis of pancreatic cyst or pseudocyst. We received 1066 unique cases from October, 2003 through February, 2011. Of these, we included in our study those cases that had K-ras analysis and/or came to a definitive diagnosis (surgical specimen), which included 85 unique cases. Some of these patients had one or more follow-up EUS exams, which was often accompanied by cyst fluid analysis, for an additional 42 cases. This provided us with 127 total cases. Results: K-ras gene mutation was analyzed in 40 cases (31%). Of these, 18 (45%) were positive, 21 (53%) were negative, and 1 (2%) was non-diagnostic. Of the 40 patients who were tested for K-ras mutation, 5 went on to have a definitive diagnosis. All 5 cases had pre-malignant lesions - three of which were in patients with a detected K-ras mutation. The remaining two cases tested negative for the mutation, but had cyst fluid CEA values of 11,000 ng/ml and 2,690 ng/ml. Of the 87 cases where K-ras was not analyzed, 47 (54%) went on to have surgery. Of these, the final pathological diagnoses included 13 (28%) benign lesions and 34 (72%) pre-malignant or malignant lesions. Of the 57 cases where cytology was unavailable or not diagnostic, K-ras analysis was performed 21 times, 6 of which tested positive for the mutation. Conclusion: All five cases that were analyzed for K-ras mutation and came to a definitive diagnosis showed pre-malignant pathology. Although two of these cases did not detect K-ras mutations, their CEA levels were elevated to well over ten times the upper limit of 192 ng/ml accepted for predicting mucinous cysts. On the other hand, 28% of cases that were not tested for K-ras and came to a definitive diagnosis had benign lesions. The data shown here is insufficient to draw any large-scale conclusions, and further studies on a larger scale are needed. Following these set of patients into the future may also elucidate the behavior of different cysts. Disclosure: Dr. Wahid Wassef: Boston Scientific - HonorariumTable: Table. K-Ras gene mutation status and relationship to other clinical data