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, fo...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.展开更多
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
文摘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.
