Background. There has been extensive use of serum tumor markers in diagnosing pancreatic adenocarcinoma. There is no tumor marker, however, that alone has sufficient diagnostic accuracy. It is necessary to know which combination of tumor markers should be used to detect pancreatic cancer, with respect to clinical usefulness and cost effectiveness. Methods. Serum levels of 17 kinds of tumor markers were determined in 145 patients and 40 healthy volunteers. Thirty‐five patients with proven pancreatic adenocarcinoma, and 32 with benign pancreatobiliary disease (14 chronic pancreatitis and 18 biliary stones) were selected. For analysis of the usefulness of each tumor marker to differentiate these two groups, scatterplot and relative operating characteristic (ROC) analyses were used. A multivariate discriminant system to differentiate these two groups was developed using stepwise discriminant analysis by backward elimination selection. Results. The significance of each tumor marker varied according to the tumor volume. By ROC analysis, the markers were divided into four subgroups according to their usefulness in discriminating pancreatic adenocarcinoma from benign pancreatobiliary disease. A discriminant system consisting of two different discriminant functions using nine tumor markers (CA 19–9, DUPAN‐2, TPA, elastase‐1, lipase, amylase, γ‐glutamyl transpeptidase, alkaline phosphatase, and lactate dehydrogenase) was developed and designated CAMPAS‐P; it could differentiate between all 35 cases of pancreatic adenocarcinoma and 32 cases of benign pancreatobiliary disease. On the other hand, CAMPAS‐P showed a low positive rate in pancreatic tumors of unusual histologic type, and poor organ‐specific diagnostic ability in various digestive organ malignancies. Conclusions. CAMPAS‐P may be very useful for differential diagnosis between pancreatic adenocarcinoma and benign pancreatobiliary disease.

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Two tumour cell clones, 6D1 and 4C2 cells, which are defective both in the major histocompatibility gene complex (MHC) class I expression and in the endogenous antigen presentation, are recovered with interferon (IFN)-gamma treatment. The present study describes the ultrastructure of these cells by using scanning and transmission electron microscopy in relation to the effect of IFN-gamma treatment. The general morphology of these cells was found to be similar to each other and comparable to that of a tumour cell clone, 4A1 cells, of the same origin, normal in MHC class I expression; they exhibited a fibroblast-like appearance and had many blebs on all the cell surfaces, with desmosome-like junctions between cells. On IFN-gamma treatment, surface fine blebs appeared less, and mitochondria became more densely stained. Expression of MHC class I molecules on the cell surface was much higher in the IFN-gamma treated 6D1 and 4C2 cells than in untreated cells, when estimated by immunoelectron microscopy. The addition of an epitope peptide to these cells did not enhance the class I expression, which differed from other antigen presentation-defective cells such as RMA-S cells, nor change the cell surface morphology.

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