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)

Mice have been immunosuppressed with cyclophosphamide, cortisone-acetate, irradiation, or Ehrlich ascitic fluid (EAF) and then grafted with Ehrlich tumor or with one of the following strain-specific tumors: thymoma, methylcholanthrene-induced fibrosarcoma, B-16 melanoma, lymphatic leukaemia, and myeloid leukaemia. Immunosuppression of the host influenced very differently the growth of transplanted malignancies. The growth of thymoma and of Ehrlich tumor was regularly enhanced. The growth of fibrosarcoma and of melanoma, on the other hand, was retarded in mice pretreated with EAF and X-rays, or remained unchanged in mice pretreated with drugs. Leukaemia growth was not influenced by any immunosuppressive treatment; the only exception was enhanced growth of lymphoid leukaemia in animals pretreated with EAF. Thus different tumors grew differently in animals immunosuppressed by the same immunosuppressive agent, while different immunosuppressive treatment changed the growth of one particular tumor always in the same way. From this we concluded: (1) there is no rule as to how immunosuppression of the host will influence tumor growth; and (2) the way in which the malignant growth will be changed depends mainly upon the type of the tumor and probably not very much upon the type of immunosuppressive treatment.
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PMID:Effect of immunosuppression on the growth of six murine tumors. 15 96

The conjugation of antineoplastic drugs to monoclonal antibodies reactive with tumor associated antigens conveys selective cytotoxicity, overcoming the systemic toxicities caused by drugs during standard chemotherapy. 2'-Deoxy-5-fluorouridine, a more potent derivative of 5-fluorouracil, is an antimetabolite which exerts its cytotoxic action by inhibiting the enzyme thymidylate synthetase and as a result inhibits DNA synthesis. 2'-Deoxy-5-fluorouridine was successfully conjugated to anti-Ly-2.1 reactive with the murine thymoma ITT(1)75NS E3, I-1, and 250-30.6 reactive with human colon cancer cells using the active ester of 2'-deoxy-5-fluoro-3'-O-succinoyluridine (5FdUrdsucc). In vitro, 5Fd-Urdsucc-anti-Ly-2.1 was selectively cytotoxic against ITT(1)75NS E3 murine thymoma cells at nanomolar concentrations. The human colon carcinoma cell LIM1899 was inhibited by 5FdUrdsucc-I-1 conjugates in the range of 10(-7)-10(-8) M, as were Colo 205 cells by 5FdUrdsucc-250-30.6 conjugates. In vivo, 5FdUrdsucc conjugates were more effective than equivalent amounts of free 5FdUrdsucc. Against the ITT(1)75NS E3 murine thymoma, a single dose of 100 micrograms (5FdUrdsucc equivalents) 5FdUrdsucc-anti-Ly-2.1 resulted in 85% tumor inhibition compared to mean tumor size of control mice. Irrelevant 5FdUrdsucc conjugates failed to inhibit tumor growth. Multiple doses of 5FdUrdsucc-I-1 conjugate produced 50% growth inhibition of the moderately differentiated tumor LIM1899. In contrast, the human colon carcinoma Colo 205 was relatively resistant to free 5FdUrdsucc and 5FdUrdsucc-250-30.6 conjugates.
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PMID:Antitumor effect of 2'-deoxy-5-fluorouridine conjugates against a murine thymoma and colon carcinoma xenografts. 153 Jul 66

The expression of HLA-DR and of the receptors for transferrin and interleukin-2 was histochemically analyzed for 27 human lung carcinomas, 3 mesotheliomas, and 3 thymomas by use of the monoclonal antibodies CLONAB Tf-R, Il-2R, and LN3. In addition, a pan B-cell antibody (CD-19) and a pan T-cell antibody (CD3) were applied. The transferrin receptor was found to be expressed in all cases of adenocarcinoma, in 12/17 cases of epidermoid carcinoma, and in a similar percentage of the thymoma cases (2/3). The interleukin-2 receptor specific antibody stained positively only for 3 cases (1 mesothelioma, 1 adenocarcinoma, and 1 epidermoid carcinoma). The expression of HLA-DR could be demonstrated in a similar small percentage of adenocarcinoma and of epidermoid carcinoma, however in 2/3 cases of mesothelioma and thymoma, respectively. The CD-19 antibody stained negatively for all tumor cases, the pan T-antibody positive in 2/10 adenocarcinoma and in 1/3 thymoma. The data suggest that the transferrin receptor may play an important role in human lung tumor growth. In addition, it may be used as diagnostic aid for distinguishing mesothelioma from metastatic adenocarcinoma of lung into the pleura.
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PMID:Expression of transferrin- and interleukin-2-receptors, and HLA-DR in human lung carcinoma. 202 54

The antitumor activity of recombinant murine interferon-gamma (rMuIFN-gamma) against B16 melanoma and EL4 thymoma, which display different sensitivities in in vitro tests, was studied. In antiproliferation tests, B16 cells were highly sensitive to rMuIFN-gamma and growth was markedly inhibited at as low as 10 U/ml, whereas EL4 cells resisted treatment even at concentration as high as 10(4) U/ml. One of these two tumors was inoculated i.d. into C57BL/6 mice and then rMuIFN-gamma (10(4) units) was repeatedly injected s.c. starting 1 day after the tumor inoculation. For the B16-bearing mice, tumor growth was markedly suppressed and the mean survival period was prolonged, but cured mice were not observed. For mice bearing EL4 cells, the therapeutic effects were more pronounced and cured mice were observed. The EL4-cured mice showed in vivo protective immunity against EL4 tumors but not against P815 tumors, indicating tumor specificity. Histologically, a large number of lymphocytes had infiltrated the necrotic tumor mass. These results indicated that rMuIFN-gamma may have not only a direct effect but also an indirect effect in host-mediated murine response on the growth of murine tumor cells under in vivo conditions.
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PMID:Distinct antitumor mechanisms of recombinant murine interferon-gamma against two murine tumor models. 313 13

The effects of treating tumor-bearing mice with recombinant murine interferon-gamma (rMuIFN-gamma) and recombinant human interleukin-2 (rIL2) were compared using EL4 thymoma with the same mouse model. Successive administration of rMuIFN-gamma (10(4) units) starting 1 day after tumor inoculation was highly effective, while rIL2 (5 x 10(4) Jurkat units) starting 7 days later produced potent suppression of tumor growth leading to complete cure in about 50% of the mice treated with either of two agents. These results showed that the effectiveness of these lymphokines differed depending on the time of their administration. Furthermore, the therapeutic effect of rIL2 against tumor-bearing mouse was poorer in T-cell-deficient nude mice than in B6 mice and NK-cell-deficient beige mice, whereas the effect of rMuIFN-gamma was poorer in beige mice than in B6 and nude mice. These results suggest that the role of NK cells in the tumor regression caused by the treatment of rMuIFN-gamma is much more important than that of other activated lymphocytes, and that the antitumor activity of rIL2 may be due to the generation of T-cell-related lymphocytes. Our results reveal that combination therapy with rMuIFN-gamma and rIL2 can induce a synergistic effect on EL4-bearing mice.
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PMID:Differential efficacies of recombinant murine interferon-gamma and recombinant human interleukin 2 against EL4-bearing mice. 313 14

CE-2 is a chemically induced tumor of low immunogenicity in syngeneic BALB/c mice. Nylon wool columns eluting lymphocytes from the spleen of mice bearing clinically evident (5-mm mean diameter) CE-2 tumors (CE-2 TB lymphocytes) do not react with CE-2 cells in vitro, nor are they able to affect their growth in vivo in a Winn-type neutralization assay at 5:1 lymphocyte:tumor cell ratio. However, they become able to inhibit CE-2 tumor growth when 20 U of interleukin 2 (IL 2) in 0.4 ml are injected daily for 10 days at the challenge site. In contrast, mice injected with CE-2 cells and IL 2 only display tumor takes and growth that are not significantly different from those in controls challenged with CE-2 cells alone. This lymphokine-activated tumor inhibition (LATI) is not a peculiarity of the CE-2 tumor-host combination, because different tumors can be inhibited in this way and various TB lymphocytes can initiate it. In these experiments, IL 2-rich 25,000 to 30,000 m.w. fractions were obtained routinely from the culture supernatants of a clone of EL-4 thymoma stimulated with phorbol myristic acetate. Equally active IL 2-rich preparations were obtained from rat spleen cells stimulated with concanavalin A, or from MLA 144 gibbon lymphosarcoma spontaneously releasing IL 2. Treatment of CE-2 TB lymphocytes with various antibody and C, with 2000 rad gamma-irradiation, or fractionation on Percoll density gradients suggested that radioresistant functions of Thy-1.2+, Lyt-1.2+, Lyt-2.2- and of asialo GM1+ cells are independently involved in LATI induction. These lymphocytes inhibit tumor growth by recruiting the radiosensitive effector mechanisms of the recipient mice required for ultimate tumor destruction. CE-2 tumor inhibition by LATI leaves a specific delayed-type hypersensitivity and an immunologic memory, resulting in rejection of a second lethal CE-2 challenge in a significant number of mice.
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PMID:Lymphokine-activated tumor inhibition in vivo. I. The local administration of interleukin 2 triggers nonreactive lymphocytes from tumor-bearing mice to inhibit tumor growth. 387 Dec 10

This report describes the use of 131I-labeled monoclonal antibodies in two experimental models for tumor immunotherapy. In vitro treatment of the radiation-induced murine thymoma ITT-1-75NS with radiolabeled anti-Ly-2.1 significantly impaired subsequent tumor growth in vivo. However, in vivo treatment of this tumor, which previously had been injected into C57BL/6 mice, was unsuccessful. By contrast, in vitro treatment of a human colorectal tumor cell line (COLO 205) with 131I-labeled 250-30.6--a monoclonal antibody directed against a secretory component of normal and malignant gastrointestinal epithelium--completely inhibited subsequent tumor growth in BALB/c nude (nu/nu) mice. Furthermore, in vivo treatment of preexisting human colorectal tumor xenografts significantly impaired progressive tumor growth. Although some tumor inhibition was also produced by unlabeled 250-30.6 antibody, this response was considerably amplified by treatment with [131I]-labeled 250-30.6 (P less than .05), suggesting that in vivo treatment of human tumors with the use of 131I-labeled monoclonal antibodies may be clinically beneficial. The antithyroid drug propylthiouracil was used to reduce dehalogenation of the radiolabeled immunoglobulins in an attempt to improve their therapeutic efficacy.
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PMID:Tumor immunotherapy in the mouse with the use of 131I-labeled monoclonal antibodies. 658 53

Insulin and glucagon injected separately or simultaneously into CBA, C57BL, A, or C3Hf/Bu mice with aplastic carcinoma, fibrosarcoma, melanoma B16, Ehrlich tumor, lymphatic leukemia, or thymoma suppressed tumor growth and prolonged the mouse's mean survival time. Basic mechanistic features of growth retardation by insulin and glucagon were delineated for aplastic carcinoma and fibrosarcoma. In mice bearing these 2 tumors, stimulated plaque-forming capacity and phagocytosis were shown for these hormones. Cyclophosphamide abolished the growth retardation. Insulin- and glucagon-induced tumor suppression appeared mainly mediated by maintenance of high immune reactivity and phagocytosis.
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PMID:Retarded growth of murine tumors in vivo by insulin- and glucagon-stimulated immunity and phagocytosis. 701 67

Among 648 patients having undergone thymectomy for myasthenia, the authors observed one female in which the operation revealed a multilobular cyst of the thymus. The features of the histological structure of the cyst undoubtedly indicate its primary nature. A detailed microscopic examination of the fibrous cyst wall revealed some elements of the tumor growth having the structure of lymphocytic thymoma. In the authors' opinion, the fact of the development of thymoma in the cyst wall is an additional argument in favour of early surgical treatment of patients with myasthenia, particularly in the presence of cyst degeneration of the thymus.
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PMID:[Lymphocytic thymoma developing in the wall of a thymus cyst]. 727 10

Induction of immunity to a viral protein that had been transfected into a tumor cell line was studied. The nucleoprotein (NP) of vesicular stomatitis virus (VSV) was used as a model tumor-associated Ag after transfection into EL-4, and H-2b thymoma originating from C57BL/6 mice. The NP-transfected cell line (EL-4NP) was lysed by NP-specific CTL and was found to restimulate NP-specific CTL in vitro as efficiently as did VSV-infected macrophages. Despite both of these in vitro characteristics, C57BL/6 mice inoculated with EL-4NP did not mount a measurable NP-specific CTL response and developed a lethal tumor as rapidly as did mice given control EL-4. This lack of immunogenicity could not be explained by down-regulation of MHC class I molecules or by loss of NP; even EL-4NP cells metastasizing to the spleen kept their high restimulatory capacity and excellent target characteristics. However, once mice were immunized with VSV or with a vaccinia-VSV-NP recombinant virus they were protected against tumor growth of EL-4NP by CD8+ CTL but not by CD4+ T cells. Taken together, the failure of the tumor-associated Ag to induce a protective T cell response in vivo despite its excellent capacity to restimulate CTL in vitro may encourage adjuvant immunotherapy in cancer; even the effects of weakly immunizing tumor vaccines, e.g., recombinant viruses, may be efficiently amplified by tumor cells.
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PMID:Nonimmunogenic tumor cells may efficiently restimulate tumor antigen-specific cytotoxic T cells. 809 55


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