Overexpression of c-met in the early stage of pancreatic carcinogenesis; altered expression is not sufficient for progression from chronic pancreatitis to pancreatic cancer
Overexpression of c-met in the early stage of pancreatic carcinogenesis;altered expression is not sufficient for progression from chronic pancreatitis to pancreatic cancer作者机构:Department of Surgery and Oncology Graduate School of Medical SciencesKyushu UniversityFukuokaJapan
出 版 物:《World Journal of Gastroenterology》 (世界胃肠病学杂志(英文版))
年 卷 期:2006年第12卷第24期
页 面:3878-3882页
核心收录:
学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 100214[医学-肿瘤学] 10[医学]
基 金:Supported by a Grant-in-Aid from the Ministry of Education Culture Sports ScienceTechnology of Japan Research Fellowships of the Japan Society for the Promotion of Science for Young Scientistsa grant from the Japanese Foundation for Research and Promotion of Endoscopy
主 题:c-met', Pancreatic cancer Chronic pancreatitis Pancreatic carcinogenesis
摘 要:AIM: To investigate c-met expression during early pancreatic carcinogenesis. METHODS: We used 46 bulk tissues and 36 microdissected samples, including normal pancreas, chronic pancreatitis, and pancreatic cancer, for quantitative realtime reverse transcription-polymerase chain reaction. RESULTS: In bulk tissue analyses, pancreatic cancer tissues expressed significantly higher levels of c-met than did chronic pancreatitis and normal pancreas tissues. c-met levels did not differ between chronic pancreatitis and normal pancreas tissues. In microdissection-based analyses, c-met was expressed at higher levels in microclissected pancreatic cancer cells and pancreatitisaffected epithelial cells than in normal ductal epithelial cells (both, P 〈 0.01). Interestingly, pancreatitis-affected epithelial cells expressed levels of c-met similar to those of pancreatic cancer cells. CONCLUSION: Overexpression of c-met occurs during the early stage of pancreatic carcinogenesis, and a single alteration of c-met expression is not sufficient for progression of chronic pancreatitis-affected epithelial cells to pancreatic cancer cells.