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Detection of c-K-ras Mutations in Fine Needle Aspirates from Human Pancreatic Adenocarcinomas¹

Department of Pathology, Los Angeles County-USC Medical Center, Los Angeles, California 90033 [D. S., S. E. M., M. M. C.]; Department of Biochemistry, State University of New York at Stony Brook, Stony Brook, New York 11794 [C. A., K. F., J. D., M. P.]; Department of Biological Sciences, University of Southern California, Los Angeles, California 90089-0371 [N. A.]

Formalin-fixed paraffin-embedded tissue specimens obtained by fine needle aspiration of pancreatic masses from 47 patients were examined retrospectively for cytology and the presence of mutant c-K-ras oncogenes. Point mutations of c-K-ras in codon 12 were detected by RNA-DNA RNAse A mismatch cleavage after in vitro DNA amplification of the cellular c-K-ras sequences by the polymerase chain reaction. Of the 36 patients with pancreatic adenocarcinoma, mutant c-K-ras oncogenes were detected in 18 of 25 (72%) with malignant cytologies, 2 of 8 (25%) with atypical cytologies, and 0 of 3 with benign aspiration cytologies. The remaining 11 patients without pancreatic adenocarcinomas did not have mutant c-K-ras genes detectable by the assay. The diagnosis of pancreatic adenocarcinoma was based upon clinical follow-up. The presence of mutant c-K-ras oncogenes did not significantly affect survival in the patients studied. Mutant c-K-ras genes were found at the time of initial clinical presentation in the majority of pancreatic adenocarcinomas, suggesting an important role of the mutation in oncogenesis. In conjunction with cytology, our approach represents an application for cancer diagnosis at the molecular genetic level.

¹ This work was supported in part by NIH Grants GM36745 (N. A.) and CA38579 (M. P.).

² To whom requests for reprints should be addressed.

³ Present address: California Institute of Biological Research, 11099 N. Torrey Pines Road, La Jolla, CA 92037.

Received 6/ 6/89. Revised 8/31/89. Accepted 11/ 7/89.

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