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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sections were taken from the center, midzone, and margin of four human osteogenic sarcomas and one fibrosarcoma. Single-cell suspensions of tumors were examined in an indirect immunofluorescence assay with autologous or homologous anti-osteogenic sarcoma antisera as the intermediate reactant and fluorescein-labeled anti-human IgG as the final reactant. Cells were stained under conditions in which the fluorescence intensity was directly proportional to the density of the tumor-associated antigen on these cells. The density of tumor-associated antigen on cells from the center of the five tumor masses was low; cells from the midzone had intermediate levels of tumor antigen density, and cells at the margin had the highest levels. Similar preparations stained with polyspecific anti-HLA antisera did not demonstrate such a gradient. Since osteogenic sarcomas grow outward from the center, with the outer margin populated by the youngest cells, these results suggest that the oldest cells in the tumor bear the least tumor antigen, and the youngest tumor cells have the most. This is not compatible with theories which postulate that the immune system modulates the growth of a tumor so that only the least antigenic cells are allowed to grow. Alternative mechanisms are discussed.
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PMID:Antigenic differences among osteogenic sarcoma tumor cells taken from different locations in human tumors. 6 91

Lymphoblasts from 6 cases of acute lymphocytic leukemia showed a paucity of receptors for T-cells (E-rosettes) and B-cells (surface membrane immunoglobulin). In contrast, neoplastic lymphoid cells from 5 cases of non-Hodgkin's lymphoma demonstrated that 4 cases could be listed as B cell proliferations and 1 case as a T-cell tumor, Anomalous HLA cytotoxic reactions were observed in all 6 cases of acute lymphocytic leukemia and probably in 1 case of non-Hodgkin's lymphoma. When the HLA antisera was absorbed of its HLA specificity, lymphoblast cytotoxicity was still observed, indicating the presence of some contaminating nonHLA antibody in HLA antisera. Severson et al. (3) demonstrated the presence of anti-B-cell activity in 2 of the 4 antisera used in this study. Lymphoblasts failed to stimulate autologous peripheral blood remission lymphocytes and neoplastic lymphoid cells did not stimulate autologous peripheral blood lymphocytes in mixed lymphocyte culture, indicating the lack of a neoantigen as measured by this technique. However lymphoblasts from 4 cases of acute lymphocytic leukemia and neoplastic lymphoid cells from 2 cases of B-cell lymphoma stimulated better than they responded to allogeneic lymphocytes. The data suggest the possibility that lymphoblasts without receptors of E-rosettes and surface membrane immunoglobulin may contain B-cell antigens which crossreact with HLA antisera and vigorously stimulate allogeneic lymphocytes.
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PMID:Evaluation of anomalous HLA reactivity in the typing of neoplastic lymphoreticular cells. 7 45

The surface antigenic characteristics of human glial brain tumor (HGBT) cells were studied by complement-dependent cytotoxic antibody assays and indirect membrane immunofluorescence. Eight permanent, well-characterized cell lines derived from human gliomas were used for analysis with antisera raised by hyperimmunization of nonhuman primates (Macaca fascicularis) with glioblastoma multiforme tissue or established HGBT cells lines. Exhaustive absorption of these antisera to remove predominantly antispecies activity rendered HLA nonreactive "preabsorbed" antisera, which reacted with a large panel of gliomatous and nongliomatous human tumor cells; 1 carcinoma, 2 sarcomas, 2 melanomas, 1 neuroblastoma, and 8 HGBT cell lines. Four lymphoblastoid lines and 2 carcinomas were unreactive. After further absorption with a human osteogenic sarcoma cell line, the antisera demonstrated significant levels of reactivity for 8 tested HGBT cell lines and no longer reacted with the nongliomatous cultured tumor cells lines. Therefore, extensive absorption of nonhuman primate anti-human glioma sera removed all activity for the nongliomatous cell lines tested, but it left significant reactivity against a glial tumor cell line-associated antigen(s) present on all 8 human glioma cell lines tested.
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PMID:Surface antigenic characteristics of human glial brain tumor cells. 7 98

Melanoma-associated antigens (MAA) were isolated and their functional immunologic properties were evaluated. Spent fetal calf serum-free culture media and 3-m KCI extracts of cultured human melanoma cells grown in this medium were used as antigen sources. Ultracentrifugal flotation on KBr was used to separate MAA and HLA antigens present in the extracts or spent culture media; thus interference by histocompatibility antigens was prevented in subsequent tests of tumor antigenic activity. MAA purified in this manner retained their immunologic functions as evidenced by their ability to produce delayed cutaneous hypersensitivity reactions in patients with melanoma, specifically combine with antimelanoma xenoantibody, and elicit production of functionally specific xenoantibody. Possible structural differences between HLA antigens and MAA were considered in evaluation of the data.
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PMID:Purification and immunologic evaluation of human melnoma-associated antigens. 7 78

Studies on the HLA pattern of several human tumor cell lines by the mixed hemadsorption test and also studies on the discriminative patterns formed by a collection of sera on a number of cell lines and diploid cells have been reported elsewhere. It was noted during these studies that some sera reacted in a fashion indicating that they did not represent any of the HLA-A or -B series and probably not the HLA-C series either. The corresponding antigenic determinants were tentatively designated Ek-1 to Ek-11. The pattern of these antigens among the cell lines is given in a table and it seems apparent that the Ek-series considerably increases the cell identification potential of the typing results. So far, five of the sera determining the Ek-antigens have failed to be blocked by anti-beta-2-microglobulin, indicating that the antigens do not belong to the HLA-A, B or C series. Preparatory work for HLA-D typing is under way.
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PMID:Tissue typing of cells in culture. IV. Cell surface antigens of tumor cell lines, not obviously belonging to the HLA-system. 7 70

Rabbit antisera were prepared to chronic lymphatic leukemia (CLL) lymphocytes and were tested for their reaction with radioiodinated, solubilized, cell surface proteins of normal and CLL lymphocytes. A pooled, hyperimmune antiserum precipitated at least 16 polypeptides from both normal and CLL lymphocytes as shown by sodium-dodecyl sulfate polyacrylamide gel electrophoresis. These polypeptides varied in molecular weight from 11,000 to 180,000. None was prominent or unique to the CLL lymphocytes, although four peptide bands in the CLL cells usually showed more radioactivity than their counterparts in normal cells. Precipitation with antisera of known specificity showed that the cell surface proteins from CLL and normal lymphocytes included HLA antigens and beta2-microglobulin. IgM and IgD were found in preparations of normal cells and in cells of 3 of 5 CLL patients. Of cells from the other 2 patients, one showed only IgD and the other no Ig. An antigen-binding capacity test was employed to quantitate the antibody content of a pooled anti-CLL lymphocyte serum. The antiserum reacted with all Ig classes; however, after absorption with light chains and F(ab')2 fragments, the serum retained activity only for IgM and IgD. The absorbed antiserum bound 45 microgram IgM, 1.5 microgram IgD and 4.5 microgram beta2-microglobulin per milliliter. These data indicate that rabbit anti-CLL lymphocyte sera fail to detect a qualitatively unique tumor-specific polypeptide on the surfaces of CLL cells. However, such antisera contain antibodies to many cell surface proteins including IgM, IgD, HLA antigens and beta2-microglobulin.
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PMID:Quantitation of antibodies to IgM, IgD and beta2-microglobulin in antisera to chronic lymphatic leukemia lymphocytes. 7 57

A method for the isolation of HLA antigen molecules from normal and cancerous solid human tissue is described. The method employs anti-beta2-microglobulin (beta2m) antiserum coupled to Sepharose beads as an immunosorbent affinity medium. The anti-beta2m affinity chromatography procedure greatly purifies and selectively enriches HLA and any material that copurifies by affinity, with beta2m and/or HLA molecules. The HLA isolated by this purification procedure was used to immunize rabbits. The antisera obtained were absorbed on beta2m to remove all anti-beta2m antibody activity. The use of such anti-HLA antisera in radioimmunoassays, immunoprecipitation studies, and F(ab')2 blocking experiments demonstrated that these antisera are directed against a common HLA determinant present on the heavy (alloantigen-bearing) chain of all HLA molecules. The use of an identical procedure employing human tumor tissues has resulted in the isolation of HLA-like or HLA-associated tumor-specific antigens as demonstrated by the leukocyte adherence inhibition (LAI) assay.
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PMID:Isolation of HLA and tumor antigens by means of affinity chromatography employing anti-beta2-microglobulin (beta2m) antiserum. 8 11

The majority of melanoma tumor antigen activity present in melanoma extracts derived from fresh tumor tissue binds to a Sepharose-anti-beta2-microglobulin adsorbent. Removal of HLA antigens from the extracts of melanoma tissue by using a KBr flotation technique did not reduce either the tumor antigen activity of the extracts or the binding of melanoma tumor antigen (MTA) activity to the Sepharose-anti-beta2-microglobulin adsorbent. The complete blocking of MTA activity by pretreating the anti-beta2-microglobulin adsorbent with beta2-microglobulin and the lack of detectable MTA binding to a Sepharose anti-normal human serum adsorbent demonstrated the specificity of the binding of MTA to the anti-beta2-microglobulin adsorbent.
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PMID:Association of melanoma tumor antigen activity with beta2-microglobulin. 8 15

Evidence for tumor-specific transplantation antigens of human prostate carcinoma was gained by others from in vivo sensitization. The fact that these antigens have not been detected by in vitro methods prompted us to investigate whether EB 33 cells, originated from a human prostate carcinoma by one of us (F.H.S.), expressed these antigens. Using 3-M potassium chloride extracts of EB 33 cells for immunization of New Zealand white rabbits, we obtained xenogeneic antibodies. Further analysis of their specificity was achieved by indirect immunofluorescence and by measurement of their cytotoxicity in a [51Cr]-release test. Xenogeneic antibodies were cytotoxic for EB 33 cells. However, the extent of cell lysis depended on the passage number of EB 33 target cells, thus reflecting an alteration of the antigenicity of the EB 33 cell population during culture. Formation of nonspecific antibodies could be absorbed with HeLa cells. As HLA were not detectable on EB 33 cells, results obtained from absorption experiments with homogenates of normal and malignant prostate tissue may argue for organ-specific and tumor-related transplantation antigens on EB 33 cells.
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PMID:Antigenic properties of a cell line from human prostate carcinoma (EB 33). 8 66

We describe the establishment and characterization of WiDr, a cell line derived from a human colon carcinoma. It produces carcinoembryonic antigen in culture, and has a doubling time of 15 hr with plating efficiency of 51%. The HLA antigenic profile and the allozyme genetic signature (composed of eight gene-enzyme systems) of WiDr cells are different from those of HeLa cells. Furthermore, WiDr cells possess three marker chromosomes, again distinct from the HeLa marker chromosomes. Finally, it is highly tumorigenic in four different xenogeneic animal models. Based on these studies, WiDr represents a useful model cell line for tumor cell biology investigations.
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PMID:Characterization of the WIDR: a human colon carcinoma cell line. 9 12


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