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doi: 10.1093/jnci/64.3.CO3pmid: N/A
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doi: 10.1093/jnci/64.3.CO3pmid: N/A
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doi: 10.1093/jnci/64.3.401pmid: N/A
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doi: 10.1093/jnci/64.3.403pmid: N/A
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doi: 10.1093/jnci/64.3.405pmid: N/A
Article PDF first page preview Close This content is only available as a PDF. Author notes Editor's note: Periodically, the Journal publishes solicited guest editorials as a means of transmitting to investigators in cancer research the essence of current work in a special field of study. The Board of Editors welcomes suggestions for future editorials that succinctly summarize current work toward a clearly defined hypothesis regarding the causes or cure of cancer.
Wood, Gary, W.;Morantz, Robert, A.;Tilzer, Seth, A.;Gollahon, Katherine, A.
doi: 10.1093/jnci/64.3.411pmid: N/A
Abstract Fifteen human central nervous system tumors of various histopathologic types were assessed qualitatively and quantitatively by indirect immunofluorescence for the presence of in vivo bound IgG, IgA, and IgM. The tumors were selected to reflect varying degrees of infiltration with Fc receptor-positive macrophages. The major purpose of the study was to determine the relative contribution of immunoglobulin (Ig) bound to tumor cells as compared to Ig bound to the Fc receptor-positive host macrophages. Of the 15 tumors, 1 tumor contained no detectable IgG, IgA, or IgM, 2 tumors contained only IgG and IgA bound in a smooth, homogeneous pattern to the surface of tumor cells, and 8 contained only IgG, IgA, and IgM attached to Fc receptor-positive cells. Four tumors contained significant numbers of tumor cells with cytoplasmic Ig, and two of those tumors also were infiltrated with Fc receptor-positive cells with membrane-associated Ig. Ig was removed from Fc receptor-positive cells but not from tumor cells by prolonged washing of sections of tumor at 37° C, which suggested that Ig was associated with Fc receptors. That possibility was strengthened by the observation that the IgG subclass distribution of the Fc receptor-associated Ig was predominantly IgG1 and IgG3, whereas no predominant subclass existed for IgG bound to tumor cells. Furthermore, the Fc receptor-associated Ig appeared to be in the form of antigen-antibody complexes because it had a granular quality and because IgA and sometimes even IgM were involved in the Fc receptor-bound complexes. 2 Supported in part by Public Health Service grant CA19333 from the National Cancer Institute and by institutional research funds from the Veterans Administration. 3 Research procedures were in accord with the ethical standards of the Human Subjects Committee, University of Kansas Medical Center. This content is only available as a PDF.
Ichiki, Albert, T.;Quirin, Yvonne, P.;Collmann, I., Reid;Sonoda,, Takuo;Krauss,, Stephen
doi: 10.1093/jnci/64.3.419pmid: N/A
Abstract Leukocyte adherence inhibition (LAI) assays were performed to test whether peripheral blood leukocytes (PBL) from patients with colorectal cancer could be inhibited from attachment to a glass surface when tumor-associated antigens (TAA) of human colorectal tumors were present. The assays were performed with PBL from 41 patients with adenocarcinoma of the colon or rectum with 3-M KCI extracts of colorectal tumors. The results demonstrated the presence of colorectal TAA in the 3-M KCI extract of colorectal tumor materials. The reactivity of leukocytes from patients with a favorable prognosis showed an increasing LAI trend; the reactivity of leukocytes from patients with an unfavorable prognosis had a decreasing LAI trend. In individual patients, alterations in the sequential LAI results paralleled changes in the clinical status, which thus strongly indicated that the LAI assay could be of value in the assessment of antitumor immunity. 2 Supported in part by Public Health Service General Research Support Funds and by the Physicians Medical and Educational Research Foundation. 3 Presented in part at the Annual Meeting of the American Association for Cancer Research, Denver, Colo., May 1977, and presented in part at the Fifth Chicago Symposium, Chicago, Ill., September 1978. 4 Research procedures were in accord with the ethical standards of the Committee on Research Participation, University of Tennessee/Knoxville. This content is only available as a PDF. Author notes 8 We acknowledge the cooperation of Dr. F. S. Jones, Dr. A. A. Kattine, Dr. J. H. Evans, Dr. F. K. Patterson, and Dr. J. V. Lewis in providing colorectal tumor materials. We also acknowledge Ms. Kathy Wenzel, Ms. Sallie Macy, and Ms. Geraldine Brabson for obtaining the blood specimens; and Mr. Frank Norton, Mr. John MacGuire, and Mr. Kent Smith for expert technical assistance.
Wiseman, Charles, L.;Bowen, James, M.;Davis, James, W.;Hersh, Evan, M.;Brown, Barry, W.;Blumenschein, George, R.
doi: 10.1093/jnci/64.3.425pmid: N/A
Abstract Cellular immune responses to antigens associated with mouse mammary tumor virus were evaluated in 101 human female subjects with the use of the lymphocyte blastogenesis assay. Positive responses (stimulation index, >3.0) were seen in 18 of 61 (30%) breast cancer female patients and 2 of 21 (9%) normal female controls. Not only did breast cancer patients respond more frequently but also their stimulation indices were substantially higher than those of the control group. The differences between the two populations had a high degree of statistical significance (P<0.002, t-test; P<0.017, Mann-Whitney U test). Positive responses were not explainable as nonspecific cross-reactivity because simultaneous tests with Rauscher murine leukemia virus or normal mouse tissue antigens failed to reveal correlating lymphocyte stimulation. Ordinary contact with patients did not appear to influence the frequency of positive cellular responses on the part of normal women. However, female laboratory workers, presumably in contact with mice or mouse viruses, showed frequent reactivity and thus were not considered normal controls. Frequently, reactivity (3/10 subjects) was also seen in a small panel of women with a history of benign breast disease. The study revealed a highly significant association between human breast cancer and in vitro cellular responses to mouse mammary tumor virus, as documented by the lymphocyte blastogenesis assay. Because selected normal populations also showed reactivity, further studies with this technique should be conducted with careful scrutiny of possible environmental, genetic, and clinical correlations among the tested subjects. 2 Supported in part by Public Health Service (PHS) grant CA16789 from the National Cancer Institute and by PHS Institutional Research Grant Committee award RR5511-16 from the Division of Research Resources, National Institutes of Health. 3 Research procedures on human experimentation were in accordance with the ethical standards of the Surveillance Committee, M. D. Anderson Hospital and Tumor Institute, The University of Texas System Cancer Center. This content is only available as a PDF. Author notes 8 We are grateful to Ms. Betty Robinson and Mr. James B. Waldron for their expert technical assistance and to Dr. Earl Ritzi, University of Tennessee Center for the Health Sciences (Memphis, Tenn.) for performing gp52 determinations.
Fukuda,, Mamoru;Wanebo, Harold, J.;Tsuei,, Lillian;Ashikari,, Roy;Sarkar, Nurul, H.
doi: 10.1093/jnci/64.3.431pmid: N/A
Abstract The direct leukocyte migration inhibition (LMI) test was done with leukocytes from healthy women and from patients with primary operable breast cancer, benign breast disease, or head and neck cancer. Purified preparations of murine mammary tumor virus (MuMTV), Mason-Pfizer monkey virus (MPMV), and murine leukemia virus (MuLV) were used. For each virus, the lowest 10th percentile of the LMI responses of controls was used to discriminate positive from negative responses. Leukocytes from 46 of 94 (49%) breast cancer patients responded to MuMTV, which was significantly different from each of the other test groups: Positive reactions were observed in only 9 of 67 (13%) healthy persons, 2 of 32 (6%) patients with benign breast tumors, and 2 of 20 (10%) patients with head and neck cancer. Although leukocytes from 29% of the breast cancer patients responded to MPMV, this response did not significantly differ from that observed in healthy women (14%), in patients with benign disease (20%), or in patients with head and neck cancer (20%). The leukocytes from the breast cancer patients were not reactive to MuLV. LMI tests to both MuMTV and extracts of MCF-7 cultured breast cancer cells were done in 36 breast cancer patients and 40 healthy women simultaneously. Of the breast cancer patients, 75% responded to MuMTV and/or MCF-7 antigen as compared to 18% of the controls (P<0.005). These data suggest that leukocytes from breast cancer patients are presensitized to MuMTV and antigen(s) present in MCF-7 breast cancer cell line, but not to MPMV or MuLV. 2 Research procedures were in accord with the ethical standards of the Human Investigation Committee of Memorial Sloan-Kettering Cancer Center. This content is only available as a PDF.
Hager, Jean, C.;Gold, David, V.;Barbosa, James, A.;Fligiel,, Zuzana;Miller,, Frederick;Dexter, Daniel, L.
doi: 10.1093/jnci/64.3.439pmid: N/A
Abstract Cultured human colon carcinoma cells were induced by the polar solvent N,N-dimethylformamide (DMF) to express a more differentiated phenotype as indicated by three types of antigen markers. Carcinoembryonic antigen expression in all DMF-induced cell lines was enhanced. Exposure of cells to DMF resulted in a reduction in ability to bind antibody to tumor-derived colon mucoprotein antigen (CMA) with a concomitant gain in binding of antibody to normal CMA. DMF-induced differentiation was further indicated by modulation of blood group antigen expression. DMF treatment decreased the amount of expression of the H-gene determinant. When DMF-treated cells were cultured in the absence of DMF for 14 days, the levels of expression of the antigen markers reverted to those characteristic of their untreated counterparts. 2 Supported by Public Health Service grants CA13943, CA20892, CA17518, CA23225, and CA21930 from the National Cancer institute and by institutional grant ACS-IN 45 0 from the American Cancer Society. 3 Research procedures were in accordance with the ethical standards of the Human Subjects Committee, Roger Williams General Hospital. This content is only available as a PDF. Author notes 9 We thank Dr. Paul Calabresi for his support of this work; Dr. I. Davidsohn for providing detailed protocols for the specific red blood cell adherence (SRCA) test; Dr. I. Diamond for supplying the outdated blood for the SRCA test and for use of the facilities of the Department of Pathology of the Roger Williams General Hospital; and Dr. Gloria Heppner for many helpful discussions.
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Abstract Sixty-seven human tumor cell lines and 15 lines derived from normal tissue were examined for the production of the oncodevelopmental markers carcinoembryonic antigen, alpha and beta subunits of chorionic gonadotropin, placental and nonplacental forms of alkaline phosphatase, γ-glutamyltransferase, cystyl aminopeptidase, and calcitonin. Both intracellular and extracellular levels of these markers were determined at three phases during the growth of each culture. Sixty-eight percent of the cell lines produced elevated levels (≥90th percentile) of at least one marker. Of those, 46% produced elevated levels of one marker only, 29% produced two, 22% produced three, and 4% produced four markers. No cell line produced more than four markers at elevated levels. In most instances, however, the expression of any two particular markers was discordant. For approximately 50% of the possible marker pairs, Spearman rank-ordered correlation analyses showed significant negative correlations, indicating that when one marker was produced at elevated levels by a given cell line, other markers were usually absent or produced at relatively low levels. In no instance was a significant positive correlation found between two markers. These data indicated that, although most human malignant cells examined produced one or more oncodevelopmental gene markers at elevated levels, no predictable coexpression of any two of the markers was seen. 2 Supported by Public Health Service contracts N01-CO75380 from the Office of the Director, National Cancer Institute (NCI), to Litton Bionetics, Inc., and Y01-CP80500 from the Division of Cancer Cause and Prevention, NCI, to the Office of Naval Research via the University of California. This content is only available as a PDF. Author notes 7 We thank Mr. Charles Riggs and Ms. Lenita Thibault for their valuable aid in statistical analyses and computer programming and also Dr. Ward D. Peterson, Jr. (Children's Research Center of Michigan, Detroit, Mich.) for isoenzyme and immunofluorescence characterizations of our cell lines. Certain radioimmunoassay agents were provided through the Hormone Distribution Program, National Institute of Arthritis, Metabolism, and Digestive Diseases. The expert technical assistance of Ms. Mindy Dunn, Ms. Nancy Addison, Ms. Christie Dapper, Ms. Kimberly Meade, Ms. Ruth Bowlus, Ms. Amalia Levy, and Mr. David Daniels is gratefully acknowledged, as is the excellent editorial assistance of Ms. Jo Ann Tichnell and Ms. Sally Miller.