Schulz H J
Institut für Pathologie, Universitätsklinikum Charité, Medzinische Fakultät der Humboldt-Universität, Berlin, Deutschland.
Zentralbl Pathol. 1994 Aug;140(3):203-10.
The bad prognosis of exocrine pancreas carcinoma manifests itself by a high incidence of recidivation, early metastasis formation and a low 5-year survival rate of 1-2% on an average has not essentially been improved in recent times although progress is evident in diagnosis as well as in surgical, radiological and cytostatic therapy. The unfavourable course of illnesses is due to the symptomless early phase rather than the existing diagnostic potential. Thus, a recording, standardization and definition of pancreatic duct atypias is a necessity for optimizing the pattern of examinations. Topographically, the structure of pancreatic parenchyma may be classified by 1) interlobular ducts; 2) intralobular ducts; 3) intercalated ducts; 4) centroacinar cells, and 5) acinar cells. Based on this matrix, entities of varying diagnostic relevance may be derived, i.e. 1) orthological histiomorphological tissue formations; 2) hyperplastic epithelial changes; 3) metaplastic epithelial formations; and 4) atypical hyperplasias. Beyond this, there are numerous indications of a redifferentiation of numerous pancreatic cell types, primarily of acinar cells. The close relationships between ductal and acinar cells may be subsumed as a terminal ductulo-acinar intercalated duct complex. Against the background of chronic pancreatitis and corresponding length of history (< 6.5 years), cancer may develop in up to 16% of cases. On the molecularbiological level, point mutations of the K-ras gene, a mutation or deletion of the p53 suppressor gene and an excess production of the c-erbB-2 protooncogene are found in a great number of pancreatic carcinomas.(ABSTRACT TRUNCATED AT 250 WORDS)