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

Antibody-dependent lymphocyte cytotoxicity against human colon carcinoma cells grown in vitro was demonstrated with rabbit anti-carcinoembryonic antigen (CEA) antisera and normal human lymphocytes. The same antisera produced no tumor cell lysis in a complement-dependent cytotoxicity test. The specificity of the reaction was demonstrated by the inhibition of antibody-dependent lymphocyte cytotoxicity after the addition of increasing amounts of purified CEA to the antiserum and by the fact that only tumor cell lines expressing CEA on their surface were lysed. Antibody-dependent lymphocyte cytotoxicity was also observed against two colon carcinoma cell lines that expressed Blood Group A antigen, using a human serum containing anti-Blood Group A antibodies of the immunoglobulin G class. This reaction was specifically inhibited by absorption with Blood Group A red cells, whereas the anti-CEA-dependent cytotoxicity was not inhibited by absorption with red cells of different blood groups.
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PMID:Antibody-dependent cell-mediated cytolysis of human colon carcinoma cells induced by specific antisera against carcinoembryonic antigen. 87 92

Antibody dependent lymphocyte (K cell) mediated lysis of tumor cells in vitro was used to assay for cell surface associated carcinoembryonic antigen (CEA) and two CEA-related normal tissue components, "normal glycoprotein" (NGP) and biliary glycoprotein I (BGP I). Three tumor cell lines were used as target cells. These were HT-29, colon carcinoma, T-24, urinary bladder transitional cell carcinoma and Mel-1, malignant melanoma. To induce lysis we used the IgG-fraction of specific rabbit and monkey anti-CEA sera and of specific rabbit anti-NGP and anti-BGP I sera, respectively. Purified human lymphocytes were used as effector cells. HT-29 was efficiently killed by low concentrations of rabbit anti-CEA and less efficiently by monkey anti-CEA. T-24 and Mel-1 were not lysed by anti-CEA, HT-29 and T-24 were lysed by low concentrations of anti-BGP I. In contrast only HT-29 was lysed by anti-NGP. Only a fraction of the tumor cells was killed by the different antisera although kinetic studies showed that the lytic reaction was complete well before the end of the eighteen hour incubation period used in the assay. Anti-CEA and anti-BGP I gave 30-40% corrected lysis of HT-29. With anti-NGP the corresponding figure was 10-20%.
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PMID:K cell mediated lysis of cultured colon carcinoma and urinary bladder carcinoma cells induced by monospecific antisera against carcinoembryonic antigen (CEA) and two CEA-related normal glycoproteins. 87 41

Chemically induced bowel tumors in Wistar/Furth (W/F) rats possess surface antigens analogous to those demonstrated in humans with colon carcinoma. To determine if these in vitro tumors markers have any in vivo significance, tumor isograft challenge experiments were performed. Groups of animals received three immunizing doses of 10(7) cells from chemically induced colon carcinomas NG-W1, DMH-W49, or DMH-W9 or small-bowel adenocarcinoma DMH-W7. Control rats were immunized with a noncross-reacting, virally induced mammary fibroadenoma A9-W1. Six weeks after immunization, all animals were challenged with 1 X 10(5) or 3 X 10(4) colon carcinoma NG-W1 cells. None of the NG-W1-immunized animals developed tumors after either NG-W1 challenge dose. In contrast to this strong protection by "private" tumor rejection antigen (TRA), protection by common or "tissue type specific" antigens was evident only if tumor volumes were measured. Twenty-two days after low-dose NG-W1 challenge, mean tumor volume (m) in animals immunized with colon tumor DMH-W9 (m=0.25 cu cm) and DMH-W49 (m=0.17 cu cm) were less (p less than 0.05) than in animals untreated (m=1.0 cu cm) or immunized with mammary fibroadenoma A9-W1 (m=0.9 cu cm). Embryonic antigens also may function as weak TRAs. NG-W1 challenge tumor volumes in fetal-gut-immunized (m=0.9 cu cm) and whole embryo-immunized animals (m=0.9 cu cm) were less (p less than 0.05) than in fetal-kidney-immunized (m=2.5 cu cm) or adult-colon-immunized animals (m=1.8 cu cm). Low-dose NG-W1 challenge tumor volumes were less (p less than 0.01) in multiparous females (m=0.3 cu cm) than in either untreated (m=1.2 cu cm) or age-matched virgins (m=1.4 cu cm). In vitro tumor markers in this model may serve an important function in vivo as TRAs.
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PMID:Cell surface antigens in a rat colon cancer model: correlation with inhibition of tumor growth. 87 53

Human cell lines derived from a melanoma and a colon carcinoma, and cultures of human melanocytes and intestinal epithelial cells, as well as a mouse mesenchymal non-neoplastic cell line and a malignant subline of the same have been quantitatively studied in tissue culture for their sensitivity to thymidine. All three tumor lines produced solid tumors when injected into nude thymus-deficient mice. No tumors were obtained by injecting cells of the human normal long-term cultures or the non-neoplastic mouse line. The tumor-producing lines showed a greater sensitivity to the lethal effects of high concentrations of thymidine than their non-tumor-producing counterparts. Less than 23% of the tumor cells survived 72 hours in the presence of 1 mg/ml of thymidine, in contrast to 60% or more of the non-tumor cells. Colony formation was much more inhibited by thymidine and the differential between normal and tumor cells was even more pronounced. Tumor cells which also were treated for 72 hours with 1 mg/ml of thymidine and then plated in fresh medium formed very few colonies. If the plating efficiency of the untreated controls is considered as 100%, 4.3% or less of the treated tumor cells formed colonies, in contrast to 33% or more of the non-tumor cells.
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PMID:Selective lethal effect of thymidine on human and mouse tumor cells. 90 80

Allogeneic immune RNA (I-RNA), extracted from the peripheral blood lymphocytes of patients putatively cured of cancer, mediated cytotoxic immune reactions that apparently were directed specifically against human tumor-associated antigens. I-RNA was extracted from the peripheral blood lymphocytes of patients with various types of cancer. Patients selected had not been previously sensitized to HL-A or other normal transplantation antigens or to blood group antigens. Normal human peripheral blood lymphocytes were incubated with these allogeneic I-RNA preparations and tested for cytotoxicity against human target cells in vitro. Allogeneic I-RNA mediated cytotoxic immune reactions only against tumor target cells of the same histologic type as the I-RNA donor. I-RNA's extracted from peripheral blood lymphocytes of melanoma patients mediated cytotoxic immune reactions only against melanoma cells. Similarly, only I-RNA's extracted from the lymphocytes of patients with colon cancer mediated cytotoxic immune reactions against colon carcinoma cells, and only I-RNA's from the lymphocytes of breast cancer patients mediated immune reactions against breast cancer target cells. Allogeneic I-RNA extracted from peripheral blood lymphocytes of cancer patients possibly mediated specific cytotoxic immune reactions that were directed against common tumor-associated antigens shared by human tumors of similar histologic type.
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PMID:Mediation of cytotoxic immune responses against human tumor-associated antigens by allogeneic immune RNA. 100 93

Staphylococcus aureus, strain Cowan I, contains a cell-wall substance, protein A, which combines with the Fc part of IgG in most mammalian species. It can therefore be used as a solid-phase immunoabsorbant for elimination of the reacting immunoglobulins. Since it has been shown that Cowan I could absorb out the blocking activity of sera from rats bearing isografts of polyoma-virus-induced sarcomas or chemically induced colon carcinomas, we investigated what effects Cowan I absorption of human tumor-bearer sera might have. In all tumor-bearer sera tested, from patients with melanomas or colon carcinomas, treatment with protein-A-containing staphylococci decreased the sera's ability to inhibit lymphocyte-mediated cytotoxicity in vitro. Cowan-I-treated sera from healthy controls had no effect on lymphocyte cytotoxicity. Nor did Cowan-I-treated tumor-bearer sera potentiate or "arm" normal lymphocytes against tumor target cells. There was no evidence of complement-dependent cytotoxicity with added human complement in sera from melanoma and colon carcinoma bearing patients either before or after absorption with Staphylococcus aureus, Cowan I, The concentrations of IgA, IgG and IgM were determined in sera used for in vitro tests of blocking activity and complement-dependent cytotoxicity before and after absorption. No reduction of IgA, reduction to undetectable levels of IgG and 20-30 percent reduction of IgM immunoglobulins as compared to unabsorbed sera were demonstrated.
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PMID:Absorption of blocking activity from human tumor-bearer sera by Staphylococcus aureus, Cowan I. 112 56

Colon and small-bowel tumors were induced in WF rats by treatment with one of three chemical carcinogens. Tumor occurrence and growth were monitored by multiple double-contrast examinations. Roentgenologic diagnoses and histologic examination of tumors were verified at tumor resection or autopsy. Serial serum samples from each of 11 rats were tested in microcytotoxicity assays for their ability to block the cytotoxicity of lymph node cells from rats with isografts of colon carcinoma NG-W1 against NG-W1 target cells. Sera from all tumor-bearing rats demonstrated specific blocking activity. With two exceptions, serum blocking activity preceded roentgenologic evidence of tumor. Sera of the 2 exceptional rats lacked blocking 2 and 8 weeks before tumor detection, respectively. The sera of only one animal specifically inhibited lymphocyte cytotoxicity despite consistently negative double-contrast examinations. At autopsy this rat was found to have an adenocarcinoma of the distal rectum, impossible to visualize by the roentgenologic technique used. In serum samples obtained from animals after successful tumor excision and with no radiologic evidence of recurrence, blocking activity could no longer be demonstrated. Rats that had received carcinogen but developed no tumor and had no abnormalities on double-contrast examination demonstrated no serum blocking activity.
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PMID:Sequential studies of serum blocking activity in rats bearing chemically induced primary bowel tumors. 112 25

One hundred forty-eight cases of colon carcinoma were subjected to further pathologic study. Survival was correlated with stage and grade of the tumor and with the number of involved lymph nodes. In addition, cases were assessed as to the extent of local chronic inflammatory reaction about the lesion and the degree of sinus histiocytosis in draining lymph nodes. A correlation was possible between grading, staging, extent of lymph node involvement, and survival. A substantial difference in five-year survival was shown when local inflammatory reaction was present and when sinus histiocytosis was observed. The presence of both of these factors further improved survival. An adequate evaluation of these factors, both individually and in combination, should improve our ability to assess prognosis in colon cancer.
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PMID:Prognosis in colon cancer: a pathologic reassessment. 115 57

Soluble intracytoplasmic protein fractions and solubilized tumor membrane preparations produced by 3 M KC1 or papain treatment were isolated from a 1,2 dimethylhydrazine-HC1 (DMH)-induced rat colon carcinoma, DHM-BU 1. Solubilized preparations were fractionated by DEAE cellulose and Sephadex G200 column Chromatography. Crude extracts and fractionated materials were tested for their ability to inhibit the cytotoxicyt of lymph-node cells (LNC) from rats bearing isografts of an N-methyl-N-nitro-N-nirosoguanidine (NG)-induced colon carcinoma, ng-W1...
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PMID:Tumor-associated and embryonic antigens in soluble fractions of a chemically-induced rat colon carcinoma. 117 94

In vitro assays of cell-mediated tumor immunity utilizing 51Chromium (51Cr) labelling of cultured adherent solid tumor cells were designed which allowed an effector cell/target cell incubation time of 48 h without overriding spontaneous 51Cr release. In a series of 16 consecutive experiments, blood lymphocytes from healthy human donors, from patients with tumors unrelated to the cultural tumor target cells, and from colon carcinoma and melanoma patients were tested for their cytotoxic effects on various target cell pairs, human colon carcinoma, melanoma, or skin fibroblasts. The same reagents were used in simultaneously performed microplate and 51Cr assays. Results obtained by visual counting of microplate tests and by 24-h assays of 51Cr release or 51Cr retention correlated in 20/25 effector-cell/target-cell combinations. In a series of six consecutive experiments, lymph-node cells from untreated Wistar/Furth rats, and rats bearing either chemically-induced colon carcinoma NG-W1 or polyoma virus-induced sarcoma P-W13 were tested for their cytotoxicity on syngeneic rat colon carcinoma and sarcoma target cells. Criss-cross type experiments were performed by microplate and 15Cr techniques done in parallel. Results obtained by visual counting of microplate tests and by 48 h assays of 51Cr release or 51Cr retention correlated in 15/18 effector-cell/target-cell combinations.
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PMID:A long-term 51chromium assay for in vitro cell-mediated tumor immunity. Correlation with simultaneously performed microplate assays. 117 12


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