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AIM:To detect the expression of p33~(ING1b) protein and thechange of p33~(ING1b) gene in pancreatic carcinoma and toevaluate the significance of p33~(ING1b) in pancreatic cellcarcinogenesis.METHODS:Pathological specimens from pancreaticcarcinoma and matched non-tumor pancreatic tissues wereexamined for p33~(ING1b) expression and mutation byimmunohistochemistry,polymerase chain reaction single-strand conformation polymorphisms (PCR-SSCP) and lossof heterozygosity (LOH).RESULTS:The rate of p33~(ING1b) protein expression was 85%(34/40).A single germline missense mutation was detectedin I of 40 tumors located at codon 215:TGC-TCC (Cys-Ser).Fourteen (60.9%) of 23 tumor sampies showed LOH in ailof the informative markers tested,but no mutation wasdetected in these tumors and only two of the informativetumors lacked expressions of p33~(ING1b) protein.CONCLUSION:Mutation and loss of expression are notthe main reasons for the disfunction of p33~(ING1b) in pancreaticcarcinoma,an abnormality at the level of chromosomeand/or transcription may inhibit their normal functions,potentially contributing to pancreatic cell carcinogenesis.
AIM: To detect the expression of p33 ~ (ING1b) protein and thechange of p33 ~ (ING1b) gene in pancreatic carcinoma and toevaluate the significance of p33 ~ (ING1b) in pancreatic cellcarcinogenesis. METHODS: Pathological specimens from pancreaticcarcinoma and matched non-tumor pancreatic tissues wereexamined for p33 ~ (ING1b) expression and mutation by immunohistochemistry, polymerase chain reaction single-strand conformation polymorphisms (PCR-SSCP) and lossof 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). Courtourt (60.9%) of 23 tumor sampies showed LOH in ail of the informative markers tested, but no mutation wasdetected in these tumors and only two of the informativetumors lacked expressions of p33 ~ (ING1b) protein. CONCLUSION: Mutation and loss of expression are not the main reasons for the disfunction of p33 ~ (ING1b) in pancreaticcarcinoma, an abnormality at t he level of chromosome and / or transcription may inhibit their normal functions, potentially contributing to pancreatic cell carcinogenesis.