摘要
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.
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 single- strand 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 I of 40 tumors located at codon 215:TGC-TCC (Cys-Ser). Fourteen (60.9%) of 23 tumor sampies showed LOH in ail 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.
基金
Supported by the "258" Project Foundation of Changhai Hospital,Shanghai,China
