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

Preincubation of normal human lymphocytes with human interferon for 18-24 h at 37 degrees C resulted in an increase of the activity of both natural killer (NK) cells and antibody-mediated cytotoxic cells (ADCC). The human myeloid line, K-562, which is highly susceptible to NK cells, was employed. ADCC was assessed with antibody-coated chick erythrocytes as targets. NK cells and ADCC were detected in a 4-hour 51Cr release assay. The magnitude of the enhancement was proportionate to the amount of interferon used in preincubation of the effector cells. Preincubation of tumor-target cells with interferon does not increase their susceptibility or resistance to lysis. The major effect of interferon on the cellular metabolism of the tumor-target cell is inhibition of DNA synthesis, but no direct cytotoxic effect was detected. Our findings may be important in understanding the mode of action of interferon in increasing host resistance to a variety of pathogens and tumors. This may be accomplished by inhibiting the growth of the tumor while simultaneously enhancing the natural killing mechanism for immunosurveillance.
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PMID:Interferon enhanced human natural killer and antibody-dependent cell-mediated cytotoxic activity. 57 26

Natural cell-mediated cytotoxicity in rats as well as in mice has been shown to vary consistently with age, with peak levels detectable at 5-10 weeks. The levels of cell-mediated cytotoxicity against tumor cells could be augmented in strains of inbred rats with either high or low levels of natural reactivity, by IP injection of a variety of agents, including C. parvum, LCMV, KRV, and poly I:C. The specificity of the augmented cytotoxicity appeared to be the same as the specificity of natural killer cells which are found in normal rat spleen cells. Similarly, the cells mediating the augmented cellular cytotoxicity were small, non-adherent, esterase-negative lymphocytes with Fc receptors, as are rat NK cells. The kinetics and organ distribution of the augmentation of NK activity by poly I:C and C. parvum were compared and the kinetics were found to differ, with a shorter time course of augmented activity seen after inoculation with poly I:C. These data indicate that interferon may play a central role in the augmentation of NK activity in vivo.
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PMID:Natural cell-mediated cytotoxicity in rats. II. In vivo augmentation of NK-cell activity. 62 28

A viral inhibitor(s) is released in the supernate of mixed cultures containing human or mouse lymphocytes and cells from certain lines. The inhibitor is active against a variety of unrelated viruses and is a protein that is not toxic for cells. It does not inactivate viruses directly, but inhibits viral replication through an intracellular mechanism that involves synthesis by the cells of both RNA and protein. These characteristics identify the inhibitor as an interferon. The anti-viral activity is contained in at least two molecular species, of approximately 25,000 and 45,000 daltons, respectively. In addition to the anti-viral activity, the supernates of the mixed cultures display an anti-cellular activity, the inhibition of DNA synthesis and of cell multiplication. The anti-viral and the anti-cellular activities are positively correlated in supernates from various cultures and in partially purified preparations. The human cell population responsible for interferon production is composed mainly of Fc-receptor positive, surface immunoglobulin negative, non-T-cell lymphocytes. The ability of certain cell lines to induce interferon seems to be preferentially associated with tumor origin or with in vitro transformation by certain viruses (Epstein-Barr virus, murine sarcoma virus).
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PMID:Anti-viral activity induced by culturing lymphocytes with tumor-derived or virus-transformed cells. Identification of the anti-viral activity as interferon and characterization of the human effector lymphocyte subpopulation. 65 Jan 55

Interferon, induced in lymphocytes either with viruses or cell lines, increases severalfold the natural cytotoxicity of human lymphocytes on target cell lines. Cell separation experiments support the hypothesis that interferon enhances the activity of natural killer cells rather than generating a new population of effector cells. In mixed culture of lymphocytes and cell lines in which endogenous interferon is produced, interferon mediates an enhancement of cytotoxicity that represents up to 70-90% of the observed cytotoxicity. The effect of interferon on target cells is antagonistic to the effect on the lymphocytes: the susceptibility to cell-mediated lysis of various cells upon pretreatment with interferon is decreased and in some cases almost completely suppressed. Interferon renders target cells resistant to natural killer cells acting by an intracellular mechanism which requires RNA and protein synthesis. While normal fibroblasts are protected, virus-infected cells and most tumor cells usually are not protected by interferon. Interferon by stimulating very efficient nonspecific cytotoxic cells and by protecting at the same time normal cells from lysis, might render the natural killer cell system an inducible selective defense mechanism against tumor and virus-infected cells.
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PMID:Anti-viral activity induced by culturing lymphocytes with tumor-derived or virus-transformed cells. Enhancement of human natural killer cell activity by interferon and antagonistic inhibition of susceptibility of target cells to lysis. 65 Jan 56

A purified preparation of human leukocyte interferon used at this hospital in the treatment of malignant diseases was tested for its ability to modify the spontaneous cytotoxicity of peripheral lymphocytes from healthy donors. The inhibitory effect of allogeneic lymphocytes on the (3H)thymidine incorporation of a lymphoblastoid cell line, Raji, was augmented by the presence of interferon or by pretreatment of the lymphocytes with interferon. This form of pretreatment also increased lymphocytes' capacity for reducing the number of surface-adherent tumor cells in a microassay. Moreover, lymphocytes treated with interferon exhibited an enhanced cytotoxic capacity for target cells on incubation with such cells labelled with 51CR.
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PMID:Interferon and spontaneous cytotoxicity in man. I. Enhancement of the spontaneous cytotoxicity of peripheral lymphocytes by human leukocyte interferon. 70 Aug 95

The frequent failure of the host's immunologic responses to impose restraints on tumor growth and dissemination has led to the realization that a number of factors, both immunologic and nonimmunologic, may act in concert to affect tumorigenesis. Immunologic mechanisms involved in tumor cell destruction are predicated principally on in vitro procedures, but the relevancy of these experimental observations to the actual events in vivo remains unclear and unresolved. The macrophage has been shown to be an integral segment of the immune response and to constitute an important element of the host defense against tumors. In this connection, interferon may be implicated in tumor cell destruction through macrophage activation to cytotoxicity. Studies of age-related susceptibility of New Zealand Black mice to three different carcinogens, ie, 3-methylcholanthrene, x-irradiation, and murine leukemia virus, have further emphasized the multifactorial determinants which may be operational in oncogenesis. Advances in our knowledge of tumor immunology have suggested a number of possible modalities for preventing tumors from escaping immunologic destruction and should continue to contribute to further elucidation of neoplastic mechanisms.
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PMID:Tumor immunity. An overview. 71 38

The ability of interferon-treated macrophages to kill or inhibit the growth of tumor cells is markedly influenced by the local environment. The macrophage cytotoxic effector system is regulated by serum and other environmental factors that suppress tumor killing. Prostaglandins E1 and E2, but not F2alpha reversibly inhibited the tumoricidal state of interferon-treated macrophages. Hydrocortisone was similarly active at suppressing macrophage function. Such nonimmunologically derived factors could prevent the final triggering step for macrophage-mediated tumor killing in the local environment of the tumor and may be important in the pathogenesis of progressive tumor growth.
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PMID:Cytotoxic activity of interferon-treated macrophages studied by various inhibitors. 72 6

Human fibroblast interferon (HFIF) produced on a large scale from normal diploid cell strains was highly purified and then evaluated as to its safety clinical investigation. The selective antiproliferative activity of HFIF was observed in vitro against certain human malignant cell lines and in vivo against human bladder tumors grown in nude mice. Direct injections of HFIF into metastatic melanoma lesions of two patients resulted in either the disappearance of malignant cells or the significant reduction in tumor volume.
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PMID:Human fibroblast interferon in human neoplasia: clinical and laboratory study. 72 9

The experiment described in this report was designed to study the effects of immunostimulatory therapy in cyclophosphamide-treated hybrid New Zealand mice. Autoantibodies, renal histology and neoplasms were studied in seventeen female NZB/NZW mice treated with daily injections of the potent immunosuppressive drug, cyclophosphamide. Results were compared with fifteen female NZB/NZW mice who received both cyclophosphamide and tilorone, an interferon inducer which stimulates the immune system. Fifteen control mice received saline. The controls died with spontaneous arteritis and immune complex glomerulonephritis; their mean age at death was 46 weeks. In the cyclophosphamide group anti-DNA antibodies and renal disease were suppressed. Mean longevity was prolonged significantly to 80 weeks. Two mice died of iatrogenic causes, and the remaining fifteen mice died with neoplasms. Eleven mice had multiple neoplasms; a total of twenty-seven neoplasms appeared. In mice receiving combination therapy, autoantibody responses were not suppressed. Nevertheless, glomerulonephritis was controlled partially and the mean lifespan was prolonged to 82 weeks. Eighteen neoplasms appeared in ten mice in the combination treatment group, and five mice had more than one neoplasm. The appearance of lymphomas was delayed in mice receiving two drugs. It was concluded that concurrent therapy with tilorone stimulated autoantibody production and altered the expected pattern of neoplasia in cyclophosphamide-treated NZB/NZW mice.
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PMID:Stimulated autoantibody response and increased longevity in NZB/NZW mice treated with cyclophosphamide and tilorone. 73 97

The antitumor effect of reserve polysaccharide, paramylon, from Euglena gracilis on the transplantable sarcoma-180 was examined in mice. This polysaccharide had an effect similar to that of lentinan. Paramylon, in a dose of 1 mug/g body weight, injected intraperitoneally 24 hr after tumor implantation had an inhibitory effect on the tumor growth, although without causing complete regression of the tumor. Alkaline-treated paramylon had a similar effect but at a smaller concentration than the native one. The inhibitory activity was not lost when the paramylon preparation was treated with pronase, DNase, or RNase. The antitumor effect might be a lymphocyte-mediated process. In tumors that were regressing after treatment, there was extensive outpouring of lymphoid cells with plasma cells and macrophages. A test conducted using paramylon ruled out the possibility of an interferon-mediated inhibiotry effect on tumor growth.
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PMID:Antitumor activity of paramylon on sarcoma-180 in mice. 82 42


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