p16(INK4a) alterations in gastrinomas and non-functioning islet cell carcinomas

Background/Aim: Molecular mechanisms contributing to the tumorigenesis of n euroendocrine pancreatic tumors are still poorly understood. Therfore we ev aluated the role of the p16(INK4) tumor suppressor gene for the genesis of these tumors. Methods: Ten non-functioning islet cell carcinomas and 8 gastrinomas were a nalysed for alterations in the p16(INK4a) tumor suppressor gene by SSCP, PC R based deletion assay and a methylation-specific PCR. Results: Seven (70%) non-functioning islet cell carcinomas and 2 malignant gastrinomas (25%) showed aberrant hypermethylation or homozygous deletion o f the p16(INK4a) gene. Conclusions: The p16(INK4a) tumor suppressor gene plays an important role i n the tumorigenesis of non-functioning islet cell carcinomas and malignant gastrinomas.