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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.

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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. Methods. Tissue homogenates (11‐121 μg) from endoscopically or surgically resected colorectal adenomas, carcinomas, and normal mucosae were evaluated by a commercially available ELISA (Oncogene Science, Inc. Cambridge, MA) for mutant p21ras containing arginine position 12 (arg12), valine position 12 (val12), aspartate position 12 (aspl2), and aspartate position 13 (asp13) amino acid substitutions. Portions of the same tissue from an initial series of 27 specimens also were subjected to mutant‐enriched polymerase chain reaction (PCR) and/or PCR amplification with subsequent DNA sequence analysis to validate the ELISA data. Results. Forty‐seven adenomas, 9 carcinomas, and 14 normal mucosae were assayed. Mutations were identified in 16 (34%) of the adenomas (7‐asp12, 7‐val12, 2‐asp13), 3(33%) of the carcinomas (1‐asp12, 1‐arg12, 1‐asp13), and none of the normal mucosae by ELISA. Polymerase Chain Reaction and DNA sequencing analyses demonstrated identical results for 21 of the 23 (91%) and 14 of 16 (88%) homogenates tested, respectively. The ELISA demonstrated an overall sensitivity of 80–86%, specificity of 90–92%, positive predictive value of 86–100%, and negative predictive value of 86–91%. Conclusions. The ELISA is a feasible and valid approach for identifying p21ras mutations in human colorectal adenomas and carcinomas. Cancer1995; 76:201‐9.

A human colon adenocarcinoma cell line (LoVo) established from a lymph node metastasis was used to study properties associated with invasive tumor cells. Human amniotic membranes were used as invasion barriers to select highly invasive and noninvasive subpopulations of cells from the parent LoVo line. Enriched subpopulations were compared with respect to parameters associated with invasion. The invasive cells were more invasive in vitro and more highly sialylated than either the parental or noninvasive line. Invasive cells migrated more strongly in vitro toward gradients of soluble and insoluble laminin, and their augmented migration correlated with increased adhesion and spreading on laminin-coated substrata. Invasive cells also had the highest level of specific laminin-binding activity. Thus, the invasive cells were shown to possess specific properties that correlated with their successful traversal of the human amnion membrane.

Glutamine synthetase and glutamine concentrations were compared in various rat tissues, in rat liver throughout development and during regeneration, and in transplanted tumors. There was no obvious relationship between the two components in these tissues. The enzyme increased abruptly in liver during the third week of life, but was not significantly induced by hydrocortisone nor ‘repressed’ by treatment with glutamine. Eight tumors with different growth rates all contained glutamine synthetase and glutamine in low but reasonable concentrations. One highly differentiated Morris hepatoma contained more glutamine synthetase than normal liver. There was no depression of glutamine synthetase in liver throughout the growth period of the tumors examined. Levels of free glutamine in plasma and liver were, however, significantly less than normal in the tumor-bearing rats.