Herbert Z. Kupchik

Carcinoembryonic antigen (CEA) in the diagnosis of pancreatic cancer

Twenty‐three (85%) of 27 patients with pancreatic cancer tested for CEA by the method of Gold were positive. The CEA assay was more frequently positive in patients with cancer of the pancreas than were any other diagnostic tests used, including upper gastrointestinal series,9 hypotonic duodenography,1 coeliac arteriography,2 and percutaneous transhepatic cholangiography4; 10 of 11 patients with negative upper gastrointestinal series were positive, as were three of five with negative hypotonic duodenograms, four of five with negative coeliac arteriograms, and one with negative percutaneous transhepatic cholangiograms. CEA was positive in three patients with negative pancreatic biopsies. CEA “detected” liver metastases twice as often as did liver scan: eight positives had high CEA levels (< 10 ng/ml). Since most cases had far advanced cancer, more study of early cases is needed.

Detection of p21ras mutations in colorectal adenomas and carcinomas by enzyme‐linked immunosorbent assay

Background. Point mutations of the ras protooncogene, primarily within codons 12 and 13, are commonly identified in colorectal carcinomas and large adenomas. Despite data suggesting that ras genotyping may have clinical significance with respect to colorectal cancer screening and prognosis, more widespread use has been limited because of the lack of a suitable assay system. The principal objective of this study was to assess the feasibility and validity of a qualitative enzyme‐linked immunosorbent assay (ELISA) fair detecting the four most common ras mutations in human colorectal tumors at the protein (p21ras) level.

L-azaserine induced preneoplasia in the rat pancreas. A morphometric study of dietary manipulation (lipotrope deficiency) and ultrastructural differentiation.

Putatively preneoplastic, pancreatic atypical acinar cell foci (AACF) and nodules (AACN), collectively termed atypical acinar cell lesions (AACL), were induced in male Lewis rats by L-azaserine (300 mg/kg body weight [bw] in divided doses). Rats given carcinogen and then fed a lipotrope deficient (LD) diet developed a significantly greater number of larger lesions than animals fed complete diet throughout the experiment. It is suggested that lipotrope deficiency plays a promoting role in this model of pancreatocarcinogenesis. Ultrastructural morphometric studies of AACF, when compared to control tissues, revealed the following significant results: 1) a decrease in surface area of cell cytoplasm with no change in nuclear area, and hence increased nucleus/cytoplasm (N/C) ratio; 2) a reduction in size and uniformity of zymogen granules; and 3) an increase in number of granules per μm2 of cell. The results suggest that arrested development of the AACF cells is associated with reduced cytoplasm and zymogen production per cell. AACL may be eosinophilic due to an overall increased concentration of zymogen in these hyperplastic lesions and not because individual acinar cells in the AACL contain an increased amount of zymogen or are “zymogen-rich,” as has been reported.

Dietary Cholesterol and Colon Tumorigenesis Induced by 1,2, Dimethylhydrazine or N-Methyl-N-Nitrosourea in Rats

The relationship of dietary cholesterol to bowel tumorigenesis is controversial. Lui and associates (1) used food disappearance data and age specific mortality rates for colon cancer in a descriptive epidemiologic study. By cross classification of data they observed that dietary cholesterol independently exhibited a significant direct effect with colon cancer mortality but fat and fiber did not. In a case control study of colo-rectal cancer by Jain, et al (2) multivariate analysis, with major nutrients controlled, revealed a dose responsive direct relationship for each sex between dietary cholesterol intake and colorectal cancer.

The disparity of indirect and direct zirconylgel assays for carcinoembryonic antigen

Experience with the zirconyl phosphate gel (Z‐gel) radioimmunoassays for plasma CEA levels below 20 ng/ml (the indirect method) and for levels greater than 20 ng/ml (the direct method) has shown that a disparity of values exists, caused by shifting from one assay to the other. This disparity is at least partially due to PCA‐labile proteins reacting in the direct assay. It may be constant for individual patients but varies among patients. The magnitude of this disparity is independent of the CEA level (above 15 ng/ml).