Immunohistochemical Evaluation of Ki - 67 , p53 , K - ras Expression in Chronic Pancreatitis and Pancreatic Adenocarcinoma

Kim, In Han; Lee, Don Haeng; Lee, Jin Woo; Choi, Won; Kim, Pum Soo; Kim, Hyung Gil; Kwon, Kye Sook; Cho, Hyeon Geun; Shin, Yong Woon; Kim, Yong Soo; Kim, Young Bae

Abstract

BACKGROUND/AIMS: Hyperplasia or dysplasia of pancreatic duct epithelium has been frequently found in the pancreas of pancreatic cancer or chronic pancreatitis. We hypothesized that ductal hyperplasia and dysplasia in the pancreas represent precursor lesions of cancer.
METHODS
We examined the expression of Ki-67, CEA, p53, K-gamma alpha s using the methods of H and E staining and immunohistochemical staining for 11 pancreatic cancer and 12 chronic pancreatitis specimens. For the specimens of pancreatic cancer, we classified the tissue into normal (n=7), ductal hyperplasia (n=3), dysplasia (n=4), and cancer lesion (n=ll). The tissue of chronic pancreatitis were also divided into normal (n=10), ductal hyperplasia (n=4), and dysplasia (n=5).
RESULTS
In pancreatic cancer, the Ki-67 index was 3.73+/-3.58 in normal site, 6.62+/-4.39 in ductal hyperplasia, 13.47+/-4.02 in dysplasia, and 37.03+/-10.05 in cancer tissue (p<0.05). In this study, the expression of p53 protein was observed in 78% of dysplasia and 91% of carcinoma cells but not in normal ducts and ductal hyperplasia. K-gamma alpha s was expressed in 33% of ductal hyperplasia, 67% of dysplasia, and 80% of cancer tissue but not in normal ducts.
CONCLUSIONS
These data support the hypothesis that ductal hyperplasia and dysplasia of the pancreas represent precursor lesions of cancer. These results need further evaluation of molecular study of oncogenes.