No abstract

Significant differences in cell composition between upstream and downstream parts of plaques indicate a role for arterial flow in the distribution of different cell types. The low-flow/low-shear downstream areas of plaques contain significantly more SMCs, which could provide the background for slowly progressive growth at distal ends of plaques. The significantly high number of macrophages in the upstream areas suggests a relationship between high flow/high shear and plaque instability.

Mutations in the p53 tumor suppressor gene are frequently identified in human neoplasms. These mutations may be associated with stabilization and, therefore, with overexpression of the p53 protein product as determined by immunohistochemical staining. Using a new antigen retrieval method and a polyclonal antibody to p53 (CM-1), the authors examined 48 formalin-fixed paraffin-embedded adenocarcinomas of the pancreas for overexpression of the p53 gene product. These 48 carcinomas were obtained from a series of patients with well-documented clinical histories and extensive follow-up. The carcinomas had been analyzed previously for K-ras gene mutations, tumor ploidy, and tumor proliferating index. Specific diffuse nuclear staining for the p53 protein was identified in 19 of the 48 (40%) infiltrating carcinomas examined. Focal or negative staining was seen in the remaining 29 cases (60%). In addition, 17 of the neoplasms contained synchronous in situ carcinomas; two (12%) of these displayed diffuse nuclear staining for the p53 protein. Overexpression of p53 was associated with aneuploidy (P = .05), which had been a poor prognosticator in this series of adenocarcinomas of the pancreas. Although overexpression of p53 appeared to be associated with poor prognosis (hazard ratio, 1.8; P = .07), this was not statistically significant. Overexpression of p53 was not significantly associated with K-ras oncogene mutations or tumor proliferating index. The authors conclude that overexpression of the p53 protein occurs frequently in invasive adenocarcinomas of the pancreas and in some in situ carcinomas, as well.

The nuclear tumour antigen p53 is expressed by a gene localized on the p-arm of human chromosome 17, a region frequently deleted in colon carcinomas. Using a monoclonal antibody to p53 antigen, immunohistochemical analysis of carcinomas and dysplastic tubular adenomas of the colon has been performed to study the relation between p53 expression and dysplasia or malignancy. With this methods p53 was detectable in 55 per cent of colon carcinomas (n = 29). In 8 per cent of adenomas (n = 74), focal nuclear p53 expression was found in dysplastic epithelial cells. In general, these p53-positive regions of the polyps were histologically indistinguishable from the neighbouring tubuli. Sometimes the p53-positive nuclei were found in a focus of more highly dysplastic epithelium. The results suggest that expression of the p53 gene may be part of the process of malignant transformation of dysplastic colon polyps.