AIM: To detect the expression of p33ING1b protein and the change of p33ING1b gene in pancreatic carcinoma and to evaluate the significance of p33ING1b in pancreatic cell carcinogenesis.METHODS: Pathological specimens from pancreatic carcinoma and matched non-tumor pancreatic tissues were examined for p33ING1b expression and mutation by immunohistochemistry, polymerase chain reaction singlestrand conformation polymorphisms (PCR-SSCP) and loss of heterozygosity (LOH).RESULTS: The rate of p33ING1b 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).Hourteen (60.9%) of 23 tumor samples snowea LOH 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 p33ING1b protein. CONCLUSION: Mutation and loss of expression are not the main reasons for the disfunction of p33ING1b in pancreatic carcinoma, an abnormality at the level of chromosome and/or transcription may inhibit their normal functions,potentially contributing to pancreatic cell carcinogenesis.