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SummaryMouse ascites tumor cells exposed to specific anti-sera in the presence of complement failed to concentrate and incorporate labeled amino acid into gross cellular protein. Inhibition of amino acid uptake by specific anti-sera closely parallels cell rupture by anti-sera (in the presence of complement) and this appears to be a rapid and sensitive biochemical assay for antibody produced against mouse ascites tumor cells by the rat.

Plasma CEA levels have been determined in 92 normal women and 768 women with benign or malignant breast diseases. Only one of 92 normal women had a CEA level above 5 ng/ml. Of 253 women with benign breast diseases (gross cystic disease, adenofibroma, fibrosis, etc.) only one had a CEA level above 5 ng/ml. Ninety-four percent of the above two groups of women had CEA levels below 3 ng/ml. Of 164 women operated upon for Columbia Clinical Classification Stage A or B breast carcinoma, preoperative CEA levels were above 5 ng/ml in seven (4%). Patients with a preoperative CEA level above 3 ng/ml seemed to have an increased incidence of tumor recurrence. Elevated CEA levels (greater than 10 ng/ml) in our postmastectomy population of 288 patients have correlated with development of metastases in 14 of 46 subjects. Of 216 patients under treatment for metastatic breast carcinoma, CEA levels above 10 ng/ml have been detected in 15 percent of patients with soft tissue metastases, 38% of patients with visceral metastases and 50% of patients with osseous metastases. Of metastatic breast carcinoma patients with CEA levels above 10 ng/ml serial measurements have correlated with the patients response to therapy, progressively increasing in treatment failures and decreasing in treatment responders.

Carcinoembryonic antigen-like substance, previously detected in large amounts in the medium from cultures of human prostatic epithelial cells, also is present in extracts of benign and malignant human prostate. By column chromatography, the prostate-derived carcinoembryonic antigen-like substance derived from cultured prostate is the same as that in tissue extracts and is distinctly different from colon-derived carcinoembryonic antigen. The molecular weight of prostate-derived carcinoembryonic antigen-like substance is estimated to be greater than 5 x 10(5). Prostate-derived carcinoembryonic antigen-like substance may be a prostate-specific substance.

A controlled prospective study was undertaken to determine if fluids which bathe malignancies may contain carcinoembryonic antigen (CEA) earlier in the course of gastrointestinal cancer than does plasma of the same patient and may offer a better means for diagnosis. CEA titers were normal (less than 2.5 ng per ml) in the plasma of 42 healthy volunteers. Normal CEA levels were also found in the plasma and in the colonic mucus of 14, the gastric juice of 18, duodenal drainage of 10, and bile of 11 normal control subjects. The colonic mucus of 3 patients with ulcerative colitis, gastric secretions of 5 benign gastric ulcer patients, bile specimens from 11 normal control subjects and from 5 gallstone patients contained CEA at concentrations below 2.5 ng per ml. Positive CEA titers were found in the fluids bathing tumors of all 23 patients with colonic carcinoma, 9 of 17 patients with gastric carcinoma, and all 6 patients with pancreatic carcinoma. In contrast, positive CEA titers were found in the plasma of only 16 of 23 patients with colon carcinoma, 6 of 17 patients with gastric carcinoma, and 4 of 6 patients with pancreatic carcinoma. Among 46 patients with gastrointestinal malignancies, CEA was detected in significant concentrations in the plasma of 26 patients and in fluids bathing tumors of 38 patients. These results indicate a significant association of adenocarcinoma of the colon with CEA-positive colonic mucus (P less than 0.01) and suggest the usefulness of assaying CEA in fluids bathing tumors for the detection of gastrointestinal malignancies.

We present findings on plasma CEA in relatives and spouses from six kindreds manifesting the Cancer Family syndrome. The CEA distributions per se were transformed to square root CEA to correct for skewness and kurtosis. Significant effects of age and duration of smoking were adjusted for by linear regression. Relatives were classified as: 1) cancer patients, 2) individuals at high genetic cancer risk (one or more first-degree relatives affected, and 3) individuals at low genetic cancer risk (no first-degree relatives affected) for statistical comparisons. Unrelated spouses were also classified into corresponding groups according to their directline mate's status. Cancer patients and relatives at high genetic risk had significantly greater mean square root CEA than relatives at low genetic risk, and, surprisingly, unrelated spouses had mean levels of square root CEA which were similar to that in the corresponding cancer risk class of their direct-line mates. Our results suggest the existence of both a genetic and connubial effect on CEA, presumably due to a common environmental agent acting in concert with the degree of genetic predisposition to oncogenesis in this syndrome.

SummaryAdenine, hypoxanthine or AICA will not reverse the inhibitory effect of aza-serine on the reproduction of J-128 cells in tissue cultures. Cells exposed to azaserine increase markedly in size with a parallel increase of nuclei size and DNA content. The drug appears to act quite similarly to certain mustards by stopping cell division between S and G2. A lesion appears in the central sphere of attraction in azaserine-treated cells, increases in size and apparently causes death of the cell.

SummaryOsgood's tissue culture J-128 may be cultured on a simple medium which does not contain preformed purine or AIC. When hypoxanthine or AIC are added to the culture medium the cells utilize th...

SummaryEvidence was presented that 9-E-6-MP is dealkylated by the human in amounts adequate to provide enough 6-MP to explain the effectiveness of this drug when it is administered to chronic granulocytic leukemia patients. 9-E-6-MP does not serve as substrate for xanthine oxidase, nor purine nucleoside phosphorylase. The possibility that the enzyme responsible for dealkylation is present in human bone marrow or neutro-phils is discussed.