BACKGROUND/AIMS: Adenomas develop only rarely in the small bowel mucosa. We particularly tried to clarify the histologic change in atypia of ampullary adenomas which are not familial polyposis. METHODOLOGY: Four adenomas, 4 adenocarcinomas, and 4 normal mucosal regions of the ampulla of Vater were investigated in this study. All cases were characterized in paraffin sections for the presence of p53 protein using the anti-p53 monoclonal antibody (DO7, Dako Corp., Glostrup, Denmark) and proliferating cell nuclear antigen using the anti-PCNA antibody (PC 10, Dako A/S, Copenhagen, Denmark). To obtain the percentages (labeling index) of PCNA, a dual wavelength imaging microdensitometer (CAS 200, Elmhurst, IL) was used. RESULTS: Transition of adenoma into adenocarcinoma was recognized in 2 of 4 cases. Labeling index of PCNA was 12.2% in normal mucosa, 41.3% in adenomas, and 66.0% in adenocarcinoma, respectively. In 2 cases with carcinoma in adenoma, labeling index was higher in carcinomatous lesion than in adenomatous lesion. p53 Protein was positive in all cases of adenocarcinoma of the ampulla of Vater, and not in any case of normal mucosa or adenoma. CONCLUSIONS: The adenoma-carcinoma sequence was morphologically recognized especially in tiny carcinoma in adenoma of the papilla of Vater. Both p53 mutation and high proliferative activity play important roles for the histogenesis of invasive adenocarcinoma.
In normal rat and human, most of the nuclei of hepatic parenchymal cells are centrally located in the cytoplasm. However, it is reported that the nuclei of hepatic parenchymal cells are situated at a deviated position on sinusoidal surfaces under pathological situations such as chronic hepatitis, hepatocellular carcinoma, adenomatous hyperplasia, or regeneration. During a study on the mechanism of extreme vitamin A-accumulation in hepatic stellate cells of arctic animals including polar bears, arctic foxes, bearded seals, and glaucous gulls, we noticed that these arctic animals displayed the nuclear deviation in hepatic parenchymal cells on sinusoidal surfaces. In this study, we assessed the frequency of hepatic parenchymal cells showing the nuclear deviation on the sinusoidal surfaces in arctic animals. A significantly higher frequency of the nuclear deviation in hepatic parenchymal cells was seen in polar bears (89.8+/-3.4%), arctic foxes (68.6+/-10.5%), bearded seals (63.6+/-8.4%), and glaucous gulls (24.2+/-5.8%), as compared to that of control rat liver (9.8+/-3.5%). However, no pathological abnormality such as fibrosis or necrosis was observed in hepatic parenchymal and nonparenchymal cells of arctic animals, and there were no differences in the intralobular distribution of parenchymal cells displaying the nuclear deviation in the livers from either arctic animals and control rats. The hepatic sinusoidal littoral cells such as stellate cells or extracellular matrix components in the perisinusoidal spaces may influence the nuclear positioning and hence the polarity and intrinsic physiological function of parenchymal cells.