Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An IgG3 murine monoclonal antibody 1G3.10 was generated against a human urinary bladder carcinoma cell line TSGH-8301. The tumor-associated antigen recognized by the monoclonal antibody is a blood group A-related substance. From fluorescence-activated cell sorter analysis, a direct cytolytic effect of tumor cells by the antibody at concentrations of more than 10 micrograms/ml was seen. The antibody could target iodine-131 to established subcutaneous human bladder carcinoma xenografts in BALB/c nude mice. Monoclonal antibody alone also showed some inhibitory effect on xenografted tumor growth. In this study, radiolabeled monoclonal antibody 1G3.10 presented more effective cytotoxicity than antibody alone from in vitro and in vivo experiments.
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PMID:Radioimmunotherapy of xenografted human bladder cancer using monoclonal antibody against blood group A-related antigen. 316 82

We have isolated and characterized a melanoma tumor-associated antigen (TAA) from the spent culture medium of a melanoma cell line. Its presence has been detected in 72% of different melanoma specimens but not in normal tissues. Because tumor antigens may stimulate or perhaps block immune reactions to cancer cells, their presence on the cell surface may be a critical factor influencing tumor growth. Therefore, to define further the immunobiological characteristics of melanoma TAA, this antigen was investigated by membrane immunofluorescence. Serum from a melanoma patient known to have a high anti-TAA antibody titer was absorbed quantitatively with lymphoblastoid cells autologous to the target melanoma cells to remove non-anti-TAA antibodies. The absorbed serum was reacted with three cultured melanoma cell lines, UCLA-SO-10 (M10), UCLA-SO-14(M), and UCLA-SO-24 (M24). Of these cell lines, M10 and M14 are known to express the antigen as assessed by radioimmunoassay. Reaction of the antibody(s) to the antigen(s) on the melanoma cell surface was detected by fluorescein-conjugated goat anti-human IgG. The reactivity of the absorbed serum was inhibited by preincubation with purified melanoma TAA. These results clearly demonstrate that melanoma TAA is expressed on the cell surface of cultured melanoma cells.
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PMID:Demonstration of a well-characterized tumor-associated antigen on melanoma cell surface. 329 43

The work described here demonstrates the importance of major histocompatibility complex class I antigens for the control of tumor growth and metastasis by the host's immune system. In certain murine tumor cells which have lost expression of H-2 class I antigens, a de novo expression of H-2 can be achieved by transfection with syngeneic class I genes. In contrast to the parental cells the transfected tumors do not grow any more in syngeneic mice, or in other cases they do not form metastases. The studies suggest that the de novo expression of the H-2 antigens renders the tumors highly immunogenic and leads to effective recognition of a tumor-associated antigen in conjunction with the transfected H-2 antigen. These conclusions were confirmed in other tumor systems. For example, separation of a heterogeneous tumor into clones expressing high or low amounts of H-2 showed that only the tumor cell with low H-2 grew well in syngeneic mice, whereas the H-2 high tumor clones were rejected. In other studies in vitro induction by IFN-gamma of H-2 antigen on H-2 negative tumors led to reduced tumor growth in vivo which was due to the increased immunogenicity. About 10% of human tumors are also low or defective for HLA class I expression and often these tumors appear to be more malignant. The class I negative tumors could either have arisen from class I low or negative tissues or are HLA loss variants which escaped the attack of the immune system. Altogether, our studies and the data of other laboratories demonstrate the important role of class I antigens for anti-tumor immunity and they suggest that modulation of class I expression by gene transfection or by induction with soluble mediators could be a useful tool for the manipulation of tumor immunity.
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PMID:The influence of major histocompatibility complex class I antigens on tumor growth and metastasis. 331 98

Lymphocytes from chickens homozygous (B2B2) at the major histocompatibility complex (MHC) were tested for cytotoxic against five types of target chicken embryo fibroblasts (CEF). Lymphocytes from B2B2 chickens bearing RSV-induced tumors lysed in vitro targets of B2B2 and B5B5 RSV-infected CEF and B5B5 normal CEF, but did not lyse B2B2 and B24B24 normal CEF. Lymphocytes from normal B2B2 chickens did not lyse any of the five types of CEF targets. Alloantisera absorption studies showed that both RSV-infected and uninfected CEF shared alloantigens, in particular B-F alloantigens, with syngeneic erythrocytes. Absorption with B2B2 RSV-infected CEF significantly lowered the titer of B2B2 anti-B5B5 alloantisera. Cross-reactivity between B5 antigen(s) and tumor-associated antigen was suggested and the nature of the cross-reactivity was discussed. It is hypothesized that this cross-reactivity prevents B5B5 chickens from recognizing the RSV-induced tumors as foreign, enhances tumor growth and leads to death of the host.
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PMID:Cross-reactivity between RSV-induced tumor antigen and B5 MHC alloantigen in the chicken. 626 25

This investigation examined the effect of soluble antigen prophylaxis on s.c. and metastatic growth of B16 variants which demonstrated either a low or high propensity to colonize the lungs (B16-F1 and B16-F10, respectively) of syngeneic C57BL/6J mice. The two variants share a tumor-associated antigen, since immunization with crude butanol extracts (CBEs) of B16-F1 cells protected hosts against s.c. challenge with either B16-F1 or B16-F10 cells. CBE from B16-F10 (CBE-F10) were unable to engender a measurable immune response against s.c. challenge with either tumor variant. Pretreatment with 100 to 300 micrograms CBE from F1 cells was also effective in reducing the outgrowth of experimentally induced B16-F1 or B16-F10 pulmonary foci. However, mice immunized with 100 micrograms CBE-F10 bore significantly more pulmonary tumors than did phosphate-buffered saline-treated controls. The enhancing and protective activities were specific for the B16 tumor and could be adoptively transferred 24 hr prior to tumor challenge by i.p. injection of 5 X 10(7) spleen cells from CBE-immunized mice. The enhancing activity in the CBE-F10 immune spleen cell population was abolished by depletion of adherent cells onto plastic. Adoptive transfer of the CBE-F10-immune adherent cell population did not affect metastatic growth, suggesting that, in this experimental system, the adherent population was not an efferent suppressor and could not recruit host elements to effect suppression. Indeed, spleen cell-mixing experiments demonstrated that only immune adherent cells combined with immune nonadherent cells could partially reconstitute the tumor growth-enhancing potential of the unfractionated CBE-F10-immune spleen cell population.
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PMID:Extraction of immunogenic and suppressogenic antigens from variants of B16 melanoma exhibiting low or high metastatic potentials. 661 49

The effects of post-operative immunization with purified tumor-associated antigen on the development of lung metastases following resection of the Lewis lung carcinoma (3LL) were studied. The soluble tumor-associated antigens were isolated from 3LL cells by detergent solubilization and purified by affinity chromatography on peanut agglutinin (PNA)-agarose. The immunization with subcutaneous injections of PNA-binding glycoproteins at early phase following resection of primary footpad tumors of 3LL resulted in a significant decrease in incidence and size of lung metastases. The delayed immunization, however, failed to suppress the development and growth of metastatic lung tumors after surgery. The suppression of postoperative development of lung metastases was found to depend on timing of immunization following local tumor resection. Splenectomy performed simultaneously with amputation of tumor-bearing leg was completely abolished the decrease in the development and growth of postoperative lung metastases in immunized-mice. Evidence of lymphoid system involvement in the control of metastatic tumor growth was also supported by the observation of in vivo tumor neutralization assay utilizing the spleen cells.
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PMID:[Role of the spleen in tumor immunity--with special reference to anti-tumor immunity induced by solubilized and purified tumor-associated antigen]. 667 68

Lymphoid cells isolated from mouse mammary tumors by isokinetic gradients were not stimulated in vitro by either phytohemagglutinin or a soluble, tumor-associated antigen extract even though splenocytes from the tumor-bearing mice were responsive to both. In in vivo Winn assays, lymphoid cells isolated from tumors markedly stimulated tumor growth rate. The effect on growth rate was abrogated by exposure of the isolated lymphoid cells to antilymphocyte serum and complement.
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PMID:Activity of lymphoid cells separated from mammary tumors in blastogenesis and Winn assays. 693 Dec 58

We have attempted to generate in vitro lymphocytes cytotoxic to a widely studied model of ovarian cancer in C3HeB/FeJ mice. These attempts were unsuccessful with either syngeneic or allogeneic spleen cells. The following experimental results demonstrated that this murine ovarian tumor lacks histocompatibility antigens. (a) Tumor cells were not lysed by allogeneic lymphocytes presensitized to H-2k spleen cells. (b) Tumor cells did not specifically inhibit the cell-mediated lysis of H-2k spleen cells by presensitized allogeneic lymphocytes. (c) Histoincompatible (H-2b or H-2d) and syngeneic (H-2k) mice all died with identical tumor growth patterns within 25, 30, or 35 days following the i.p. inoculation of 10(6), 10(5), or 10(4) tumor cells, respectively. (d) Tumor cells were not lysed by an anti-H-2k antiserum and complement. (e) Absorption of the anti-H-2k antiserum with tumor cells did not decrease the cytotoxicity of the antiserum. (f) Competitive inhibition of a radioimmunoassay and polyacrylamide gel electrophoresis of immunoprecipitate of radiolabeled tumor extracts failed to demonstrate an H-2 heavy chain, although a normal amount of beta-microglobulin was present. This lack of histocompatibility antigens may explain the failure to generate lymphocytes cytotoxic to this tumor. Thus, this murine ovarian tumor, which has a serologically detectable tumor-associated antigen and can be cured by nonspecific immunotherapy, may provide an excellent model for the study of successful immunotherapy in the absence of histocompatibility antigens and associated cell-mediated reactions.
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PMID:Lack of histocompatibility antigens on a murine ovarian teratocarcinoma. 701 76

Local hyperthermia and the hypoxic cytotoxin SR 4233 were administered to nude mice with 693 +/- 47 mm3 (mean +/- SE) s.c. HCT-8 human colonic adenocarcinoma xenografts in an attempt to enhance the antitumor effects of radioimmunotherapy. Biodistribution studies revealed preferential binding of NR-Lu-10, a murine monoclonal antibody, to the tumors compared with an isotype-matched control antibody, CCOO16-3.A single injection of 25 microCi 90Y-NR-Lu-10 significantly inhibited tumor growth (control versus 90Y-NR-Lu-10: P = 0.048). The administration of hyperthermia at 41.5 degrees C for 1 h immediately following the injection of 111In-labeled NR-Lu-10 up-regulated tumor-associated antigen expression and increased antibody uptake in the tumors by 73% (P = 0.001) without significantly affecting antibody uptake in normal tissues. However, the heat treatment did not produce a more homogeneous distribution of the antibodies in the tumors and did not significantly enhance the tumor growth delay produced by 90Y-NR-Lu-10 (P = 0.07). The administration of local hyperthermia at 43.0 degrees C for 1 h, on the other hand, had direct cytotoxic effects (P = 0.03) and enhanced the tumor growth delay produced by 90Y-NR-Lu-10 (P = 0.01). SR 4233 also enhanced the tumor growth delay produced by 90Y-NR-Lu-10 (P = 0.03). The greatest antitumor effects were observed when both hyperthermia at 43.0 degrees C and SR 4233 were administered in combination with 90Y-NR-Lu-10 (P = 0.002). No toxicity was produced by the local hyperthermia, and the only toxicities produced by 90Y-NR-Lu-10 and SR 4233 were neutropenia and weight loss.
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PMID:Local hyperthermia and SR 4233 enhance the antitumor effects of radioimmunotherapy in nude mice with human colonic adenocarcinoma xenografts. 831 9

The bispecific murine monoclonal antibody (MAb) 1A10 has specificity for the human transferrin receptor (TfR) and the human tumor-associated antigen gp40. This antibody, therefore, functions as an "antigen fork" by binding to two distinct antigens on the same malignant cell. Highly purified 1A10 inhibits the growth of cells coexpressing high levels of human TfR and the tumor-associated antigen gp40 by binding to both target antigens. In SW948 cells, the majority of 1A10 binding is via its gp40 specificity, and half-maximal inhibition of cell growth by 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay requires 20-30-micrograms/ml concentrations of 1A10. The binding of 1A10 correlates with growth inhibition in the cell lines HT-29, SK-OV-3, OVCAR-2, and OVCAR-3. The growth of OVCAR-10 cells, which express little gp40 and TfR, is not inhibited by 1A10. However, SK-BR-3 cells, which express abundant gp40 and extremely high levels of TfR, are insensitive to the effects of 1A10. In some cell lines, combined exposure to 1A10 and the iron chelator deferoxamine mesylate has synergistic antiproliferative effects. A single i.p. dose of 600 micrograms 1A10 is sufficient to achieve an estimated tumor concentration of at least 30 micrograms/ml for 7 days in C.B17/Icr-scid mice bearing SW948 human tumor xenografts. Treatment of scid mice bearing day 2 or day 4 SW948 xenografts with single or multiple 1A10 doses inhibits tumor growth in a dose-related fashion. Antitumor effects are not seen with therapy using either parental antibody of 1A10. The antiproliferative properties of 1A10 in tumor cells overexpressing gp40 and TfR suggest avenues for the development of new bispecific antibody-promoted treatment strategies.
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PMID:Binding characteristics and antitumor properties of 1A10 bispecific antibody recognizing gp40 and human transferrin receptor. 854 50


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