AIM: To detect the expression of p33^ING1b protein and the change of p33^ING1b gene in pancreatic carcinoma and to evaluate the significance of p33^ING1b in pancreatic cell carcinogenesis.METHODS: Pathological specime...AIM: To detect the expression of p33^ING1b protein and the change of p33^ING1b gene in pancreatic carcinoma and to evaluate the significance of p33^ING1b in pancreatic cell carcinogenesis.METHODS: Pathological specimens from pancreatic carcinoma and matched non-tumor pancreatic tissues were examined for p33^ING1b expression and mutation by immunohistochemistry, polymerase chain reaction singlestrand conformation polymorphisms (PCR-SSCP) and loss of heterozygosity (LOH).RESULTS: The rate of p33^ING1b protein expression was 85% (34/40). A single germline missense mutation was detected in 1 of 40 tumors located at codon 215:TGC-TCC (Cys-Ser).i-ourteen (60.9%) of 23 tumor samples snowea LUH In all of the informative markers tested, but no mutation was detected in these tumors and only two of the informative tumors lacked expressions of p33^ING1b protein.CONCLUSION: Mutation and loss of expression are not the main reasons for the disfunction of p33^ING1b in pancreatic carcinoma, an abnormality at the level of chromosome and/or transcription may inhibit their normal functions,potentially contributing to pancreatic cell carcinogenesis.展开更多
基金Supported by the "258" Project Foundation of Changhai Hospital,Shanghai,China
文摘AIM: To detect the expression of p33^ING1b protein and the change of p33^ING1b gene in pancreatic carcinoma and to evaluate the significance of p33^ING1b in pancreatic cell carcinogenesis.METHODS: Pathological specimens from pancreatic carcinoma and matched non-tumor pancreatic tissues were examined for p33^ING1b expression and mutation by immunohistochemistry, polymerase chain reaction singlestrand conformation polymorphisms (PCR-SSCP) and loss of heterozygosity (LOH).RESULTS: The rate of p33^ING1b protein expression was 85% (34/40). A single germline missense mutation was detected in 1 of 40 tumors located at codon 215:TGC-TCC (Cys-Ser).i-ourteen (60.9%) of 23 tumor samples snowea LUH In all of the informative markers tested, but no mutation was detected in these tumors and only two of the informative tumors lacked expressions of p33^ING1b protein.CONCLUSION: Mutation and loss of expression are not the main reasons for the disfunction of p33^ING1b in pancreatic carcinoma, an abnormality at the level of chromosome and/or transcription may inhibit their normal functions,potentially contributing to pancreatic cell carcinogenesis.
