Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of alien histocompatibility antigens on the cell surface of the 3-methylcholanthrene-induced BALB/c (H-2d) fibrosarcoma C-1, was investigated by serological and transplantation studied. Absorption experiments with monospecific alloantisera showed that C-1 cells expressed their original private (H-2.4 and 31) and public (H-2.3, 8, 28, and 35) specificities. C-1 cells were also able to absorb monospecific antisera directed to the private specificity H-2.23 of the H-2k haplotype, as well as antisera to the public specificities H-2.1, 5, 11 11 and 25 (H-2k and in part H-2q, H-2a and H-2b haplotypes), which are absent from H-2d normal cells. Conversely, other alien specificities (H-2.2, 17, 30, 32, and 33) were not detected on C-1 cells. The C-1 cells were also unable to absorb the activity of an anti-Ia serum (1-28) directed to 1a.1, 2 and 19 (lak) specificities. Transplantation studies showed that resistance against the challenge of C-1 cells could be induced in syngeneic BALB/c mice by preimmunization with normal tissues from C3Hf and AKR (H-2k), A (H-2a) and C57BL/6J (H-2b) strains (expressing all or some of the extra H-2 antigens of the tumor) whereas no protection was obtained with DBA/2 (H-2d) or with W/Fu rat tissues. The anti-tumor activity could be passively transferred by BALB/c lymphoid cells immune to normal C3Hf, AKR, A, and NIH (H-2q) tissues, but no protection was achieved with lymphoid cells immune to DBA/2 or to W/Fu normal rat tissues. These data indicate that foreign H-2 antigens are expressed on C-1 tumor and that they might function as tumor-associated transplantation antigen which was shown to be present and individually distinct on this sarcoma by appropriate in vivo tests.
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PMID:Expression of alien H-2 specificities of a chemically induced BALB/c fibrosarcoma. 7 Apr 14

Mouse splenic lymphocytes and lymphoid tumor cells were modified with the trinitrophenyl (TNP) group either by treatment with trinitrobenzene sulfonate (TNBS) (which covalently modifies cell surface proteins) or with TNP stearoyl dextran (TSD) (which binds to the cell by noncovalent forces). These cell preparations were compared for their ability to: (a) sensitive syngeneic splenic lymphocytes leading to the generation of cytotoxic effector cells; (b) serve as lysable targets in a 4-h(51)Cr- release assay for effector cells generated in (a); and (c) act as blocking cells in the lysis of TNBS-medified targets lysed by TNP self effector cells generated in (a). In none of these three experimental systems did TSD-medified syngeneic spleen or H-2-matched tumor cells act either as a sensitizing immunogen or as a target antigen, despite the demonstration that quantitatively equivalent mounts of TNP were exposed on the cell surface in the TNBS- and TSD-modified cells. In contrast, TNBS-modified spleen cells sensitized syngeneic lymphocytes to generate effectors against TNBS-modified syageneic targets. Furthermore, TNBS- modified, H-2-matched cells served as specific lysable targets and as inhibiting cells for such effectors. These results indicate that the manner in which TNP is associated with the cell surface is important in the immunogenicity and antigenicity of hapten-modified syngeneic stimulating cells in generating H-2-associated cell-mediated lympholysis (CML) reactions. These findings raise the possibility that a covalent or at least a stable linkage with cell surface proteins (possibly H-2- controlled products) is important for immunological function. Furthermore, these observations do not favor the dual receptor model for H-2-restricted syngeneic CML if it is assumed in such a model that one receptor is specific for the TNP moiety and the second for unmodified self major histocompatibility products.
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PMID:Specificity of cytotoxic effector cells directed against trinitrobenzene sulfonate-modified syngeneic cells. Failure to recognize cell surface-bound trinitrophenyl dextran. 7 May 1

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

A variety of immunologic approaches may be potentially useful for the immunodiagnosis of cancer. These sensitive procedures might assist in the initial detection, diagnosis, and localization of tumors, and might also be used in determining prognosis and for monitoring cancer patients for recurrence of disease after therapy. The types of approaches and some of the available information regarding their clinical usefulness are reviewed. The main emphasis with potential immunodiagnostic tests has been placed on detection of circulating tumor-associated markers. However, the detection of tumor markers in tissue cells might help in the discrimination between tumor cells and nonneoplastic cells, and also might help in the categorization of the type of cancer. Detection of depressed immunologic competence or in a subpopulation of lymphoid cells may be useful in diagnosis. Humoral or cell-mediated immune responses to tumor-associated antigens have the potential of being very sensitive, specific indicators of neoplastic disease, but most of the tests for these responses are difficult and none has yet been established for use in practical clinical situations.
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PMID:Immunologic tests in diagnosis of cancer. 7 2

Tumor cell fractions isolated from tumor lines SH-3 (breast carcinoma) and RPMI-7932 (malignant melanoma) by differential centrifugations were capable of transforming lymphocytes into cytotoxic effector cells. Lymphocytes cultured alone in human AB plasma did not become cytotoxic to tumor cells. However, when cultured with tumor cell fractions sedimented at 1000 X g(R1), 20,000 X g(R2), and 100,000 X g(R3), these lymphocytes became markedly cytotoxic to specific tumor targets in a 3.5-hr (51)Cr release assay. R2 fractions were significantly more immunogenic than were R3 fractions (p less than 0.05). Although lymphocytes sensitized with SH-3 tumor cell fractions were cytotoxic to SH-3 tumor cells, they were also cytotoxic to cells from RPMI-7932 and RPMI-8322 (malignant melanoma) tumor lines and vice versa. Cells from tumor lines HT-29 (colon carcinoma) and COLO 110 (ovary carcinoma) were significantly less susceptible to lysis by effector cells generated against SH-3. These immune cells, although capable of killing cells from tumor lines, were not able to lyse cells from autochthonous normal lymphoid lines or normal lymphocytes that have been transformed by phytohemagglutinin. Tumor cell fractions were not immunogenic at low (5- to 20-mul/0.75 ml) concentrations; an increase of 4- to 10- fold in their concentrations was usually followed by a decrease in immunization.
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PMID:In vitro immunization against human tumor cells with tumor cell fractions. 7

The differential effects of normal and immunologically primed lymphocytes on the adherence of trypsinized rat mammary adenocarcinoma tumor cells (DMBA"8) to their substratum are described, utilizing both allogeneically and syngeneically primed lymphoid cells as effectors. This observation may illustrate an important immunological phenomenon, and may result in a simplified assay procedure for the detection of cell-mediated immunity.
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PMID:Target cell - substratum interaction. I. Effect of primed lymphocytes on a rat mammary adenocarcinoma tumor cell line. 7 40

Four-hundred and fifty nine cancer patients were skin tested with extracts from five lymphoid cell lines. More than 50% of patients with lymphoma had positive skin tests with the extracts prepared from the cell line derived from Burkitt's lymphoma (BL) and more than 50% of nasopharyngeal carcinoma (NPC) patients reacted to the NPC-derived cell line extracts. Although the significant association between patient diagnosis and orgin of cell lines suggested that tumor-associated antigens were responsible for the pattern of delayed hypersensitivity, problems in standardization of antigen potency and non-specificity need to be resolved before this in vivo assay achieves its full potential.
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PMID:Delayed hypersensitivity reactions of cancer patients to antigens on lymphoid cell lines. 8 Nov 88

Immune response in WKA rats immunized with methylcholanthrene-induced KMT-17 tumor was measured by radioisotopic footpad assay. The assay was specific, quantitative, and objective compared with the ordinary method of measuring the thickness of footpads. The strongest footpad reaction was observed 24 hr after injection of the antigens. The reaction was transferred by lymphoid cells but not by serum. These results indicate that the footpad assay manifests delayed-type hypersensitivity to tumor antigens. In order to obtain more reliable antigen preparation for the footpad assay, antigens prepared by several methods were compared. Solubilized antigen extracted with sodium deoxycholate (DOC) showed the strongest reaction in the immunized host and weak reaction in the control non-immunized host. This marked difference between the immunized and control groups indicates that DOC-extracted antigen was better antigen than tumor cells treated with mitomycin-C (40 microgram/ml), formaldehyde solution (0.2%, 0.01%), X-irradiation (3,500, 10,000 rad), non-treated whole-cell antigen, crude membrane, cell homogenates, or antigens extracted by hypotonic sonication and 3M KCl method. The DOC-extracted antigen was well preserved at -20 degrees for 1 month.
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PMID:Detection of delayed hypersensitivity reaction in rats by radioisotopic footpad assay with sodium deoxycholate extract and mitomycin-C-treated tumor cells. 8 87

The dissociated cell surface membranes of a rat Moloney sarcoma (MST), derived from a BN rat, were extracted with 2 M KI, with 6 M guanidine thiocyanate, or by papain digestion. Extracts obtained with these three reagents were fractionated on columns of controlled-pore glass, 170 A pore size. A fraction was eluted from each preparation that contained tumor-associated antigens (TAA), viral, fetal, and histocompatibility antigens. With an antibody specific for TAA, the TAA, devoid of detectable viral, fetal, and histocompatibility antigens, were co-precipitated by addition of goat antibody to rat immunoglobulin. After electrophoresis, on slab gels, three bands were detected with estimated m.w. of 185,000, 150,000, and 70,000. No such bands were detected on slab gel electrophoresis with extracts of BC5, a chemically induced tumor, of normal BN lymphoid cells, of M-MuLV, or of fetuses, after incubation with anti-TAA antibody and goat antibody to rat immunoglobulin. TAA extracts prepared with 2 M KI, 6 M guanidine thiocyanate, or papain digestion showed immunologic reactivity. Cold TAA inhibited the co-precipitation of labeled TAA by rat antibody specific for TAA; they elicited antibody in guinea pigs but not in rats; and antibodies specific for TAA were cytotoxic to MST in the presence of C.
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PMID:Tumor-associated antigens of rat moloney sarcoma cells. I. Cell-surface antigens. 8 54

Natural killing (NK) in humans, as well as in other species, has been shown to be specific for antigenic determinants present on the surfaces of a variety of tumor cells. Physical separation of NK cells from K cells, which mediate antibody-dependent cellular cytotoxicity (ADCC), has not been successful; however, there is indirect evidence suggesting that these activities are distinct. To further study the relationship between NK and K cells, competitive inhibition techniques were employed. NK cells can be blocked via two mechanisms: 1) by direct inhibition with NK-sensitive tumor cells binding to NK receptor sites present on the effector cells and 2) by steric inhibition resulting from the binding of antibody-coated cells to the FcR on the effector cells. K cells, however, lack the NK receptor site(s) but are FcR+, and can therefore be blocked only by antibody-coated cells. We therefore postulate that NK and K cells are two separate lymphoid populations. NK cells bear receptor site(s) for NK determinants and FcR, whereas K cells bear only FcR.
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PMID:Natural killing and antibody-dependent cellular cytotoxicity are mediated by different mechanisms and by different cells. 8 58


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