MYC aberrations in AC and PDA

Abstract

Introduction: The aim of our study was investigation of the presence of MYC amplification in PDA and carcinoma of the vater. Method: 74 cases of PDA, 15 cases of cancer of the vater and seven cases of control pancreatic tissue were included in the study. We examined the expression of MUC1, 2 and 5AC types by immunohistochemical analyses in PDA and carcinoma of the vater. Dual-color interphase fluorescent in situ hybridization (FISH) was performed on 4-μm thick sections of formalin-fixed paraffin-embedded (FFPE) tumors. Results: Most of the PDA have been reported as - MUC1 + / MUC5AC + and accounted for 42% (31/74), the smallest was a group with the intestinal mucin phenotype (MUC2 +) and only 7% (5/74). The group with the gastric phenotype (MUC5AC +) was - 15% (11/74). Carcinoma of the vater in most cases have been reported as MUC2 + and accounted for 80% (12/15), 20% (3/15) of cases the tumor presented as MUC1 + /MUC5AC +. In normal ducts of all 7 control cases the tested loci had balanced (diploid) profile. FISH analysis of PDA revealed of MYC gene copy number in 21/74 (28%) cases. Eight of the 74 pancreatic tumors (10,8%) revealed MYC gain in association with an increased chromosome 8 copy number. Conclusion: MYC gene amplification should be considered as a marker of a more aggressive behavior in cancers biliary pancreaticduodenal region. Diploid profile MYC gene in carcinomas of the vater indicates a more favorable prognosis compared with ductal adenocarcinomas of the pancreas.