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Background  Cell cycle inhibitor and tumor suppressor gene  p16 / MTS-1  has been reported to be altered in a variety of human tumors. The purpose of the study was to evaluate primary pancreatic ductal adenocarcinomas for potentially inactivating  p16  alterations.    Methods   We investigated the status of  p16  gene by polymerase chain reaction (PCR), nonradioisotopic single strand conformation polymorphism (SSCP), DNA sequencing and hypermethylation analysis in 25 primary resected ductal adenocarcinomas. In addition, we investigated p16 protein expression in these cases by immunohistochemistry (IHC) using a monoclonal antibody clone (MS-887-PO).    Results  Out of the 25 samples analyzed and compared to normal pancreatic control tissues, the overall frequency of  p16  alterations was 80% (20/25). Aberrant promoter methylation was the most common mechanism of gene inactivation present in 52% (13/25) cases, followed by coding sequence mutations in 16% (4/25) cases and presumably homozygous deletion in 12% (3/25) cases. These genetic alterations correlated well with  p16  protein expression as complete loss of p16 protein was found in 18 of 25 tumors (72%).    Conclusion  These findings confirm that loss of p16 function could be involved in pancreatic cancer and may explain at least in part the aggressive behaviour of this tumor type.

Alterations of tumor suppressor gene p16 INK4a in pancreatic ductal carcinoma