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)

Murine spleen cells generate nonspecific cytotoxic cells, referred to as natural killer (NK) cells, within 4 d of incubation in Mishell-Dutton cultures. This NK cell type does not arise in cultures of BALB/c.nu spleen cells or in cultures of T-cell depleted C57BL/6 spleen cells, indicating that its activation depends on T cells. Another type of NK cells is induced by tumor necrosis serum in murine spleen-cell cultures. It arises within 24 h and its activation does not depend on T cells. This cell type (and its precursor) expresses the recently discovered cell-surface marker Qa5 (controlled by the Q region of chromosome 17) that distinguishes this NK cell from the NK cell that depends for its activation on thymic function. Qa5+ NK cells are also induced by interferon.
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PMID:Tumor necrosis serum induces a serologically distinct population of NK cells. 47 59

A survey of human diploid, aneusomic, transformed and tumor fibroblast or fibroblastoid cell lines for their capacity to produce interferon after polyriboinosinic acid:polycytidylic acid induction showed considerable variation in responsiveness. There was no apparent correlation between karyotype or phenotype and interferon production. Pretreating or "priming" the cells with human interferon generally led to increased yields of interferon after polyriboinosinic acid:polycytidylic acid induction in all cell lines tested. All the cells also showed the "super-induction" phenomenon, although to varying degrees. The combination of priming and superinduction conditions led to the production of very high yields of interferon in some cell lines, but in other lines, yields less than either the primed or superinduced amounts were found. A more limited survey of human cell lines for their capacity to produce interferon after Newcastle disease virus induction also showed that yields varied from line to line. However, there was little evidence to suggest that ability to produce interferon after Newcastle disease virus induction correlated with that after polyriboinosinic acid:polycytidylic acid induction.
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PMID:Interferon production: variation in yields from human cell lines. 48 24

A point mutation, called beige, on linkage group 14 in C57BL/6 mice leads to a marked impairment in natural killing and antibody-dependent, cell-mediated cytolysis (ADCC) of tumor cells. The defect in NK cytolysis was predetermined at the level of progenitor cells in the bone marrow as revealed in radiation chimeras. This impairment in NK function could not be accounted for by an altered organ distrubution, target selectivity, or ontogenesis. Interferon did not fully restore the response, which suggests that the defect may not result solely from a lack of endogenous interferon stimulation in beige mice. The frequency of target-binding cells was normal in all lymphoid organs, which suggests that the defect is intrinsic to the NK cell and does not involve an altered population size or an inability to recognize and interact with the target. Rather, the defect may lie within the lytic pathway subsequent to target cell contact. These mice should provide a useful NK-deficient system for studies of T cell or macrophage immunity and in addition they provide a means for testing the in vivo significance of NK cells in resistance to tumors and virus-infected cells.
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PMID:The beige mutation in the mouse. I. A stem cell predetermined impairment in natural killer cell function. 48 78

Sodium butyrate together with interferon enhances the antitumor effect of interferon in vivo. When Sarcoma 180 TG cells are inoculated in mice, the mean survival time and final survival rate are greatly increased compared to those for treatment with interferon alone. Similarly, a significant delay in the mean survival time is observed when mice inoculated with L1210 cells are treated with sodium butyrate and interferon. This effect could be due at least in part to a potentiation of interferon action on the tumor cells.
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PMID:Enhancement of interferon antitumor action by sodium butyrate. 49 98

Treatment of older mice with pyran copolymer, a known interferon-inducer, was found to result in a rapid boosting of cell-mediated cytolytic activity against YAC-1 tumor target cells. The effector cells were characterized as being non-adherent and were presumed to be natural killer (NK) cells. Augmentation occurred in various lymphoid organs and was detectable 2-3 days after drug treatment. Differences in the levels of boosted activity among the lymphoid organs resulted when the route of administration was varied. The degree of augmentation was largely independent of the dose of pyran, but did vary among different strains of mice. Augmentation, moreover, was followed by a rapid decline by 5-7 days.
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PMID:Augmentation of natural killer activity by pyran copolymer in mice. 52 80

Multiple myeloma can be regarded as model disease for quantification of tumor mass, investigation of tumor cell kinetics and of tumor response to therapy. The quantification of the tumor cell number allows evaluation of prognosis and monitoring of disease as well as of therapy induced responses. Treatment of multiple myeloma is primarily based on the alkylating drugs cyclophosphamide and melphalan. In recent years other cytostatic substances, also effective in the treatment of this disorder have been introduced. However, the sensitivity determination of the individual myeloma stem cells seems to be the only possible method which possibly increases the response rate significantly. In accordance with these considerations we have, in preliminary clinical investigations, observed a good correlation between the in vitro determined cytostatic drug sensitivity and the in vivo response to therapy. Further progress in the treatment of multiple myeloma is to be expected with the introduction of interferon into the therapeutic regimen. Administration of this glycoprotein has resulted in significant reduction of tumor mass in more than half of all patients treated up to this time.
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PMID:[New aspects in the clinical course determination and therapy in multiple myeloma]. 55 24

We reported earlier that the methylation of unmethylated reovirus mRNA (reo mRNAU) by the cellular methylating enzymes is impaired in extracts of uninfected, interferon-treated Ehrilich ascites tumor cells (S30INT). We find now that after the methylation of reo mRNAU has stopped in S30INT, the RNA can be reisolated and further methylated in an extract of control cells (S30C). Thus the impairment of methylation in S30INT cannot be due to cleavage or irreversible inactivation of reo mRNAU. Freshly added reo mRNAU can be methylated in S30INT in which the methylation of previously added reo mRNAU has stopped. This indicates that the impairment is due to the depletion of S-adenosylme thionine (the methyl donor), the accumulation of S-adenosylhomocysteine (an inhibitor of methylation), or the irreversible inactivation of reo mRNAU. Freshly added reo mRNAU can be methylated in S30INT in which the methylation of previously added reo mRNAU has stopped. This indicates that the impairment is not due to the depletion of S-adenosylmethionine (the methyl donor), the accumulation of S-adenoxylhomocysteine (an inhibitor of methylation), or the irreversible inactivation of the methylating enzymes. It may be due, however, to the unavailability of reo mRNAU for methylation. The extent of the impairment of reo mRNAU methylation in S30INT decreases with an increasing concentration of reo mRNAU but is not affected by added poly (U), ribosomal RNA, or encephalomyocarditis virus RNA (an mRNA that is probably not capped or methylated at its 5' end). The methylation of reo mRNAU is also impaired in an extract from cells that have not been treated with interferon but with the interferon inducer poly(I) - poly(C). The inhibitor is apparently a macromolecule that is inactivated during incubation. It decreases the methylation at the 7 position of the 5' terminal guanylate residue. In vitro, the rate of reo mRNA synthesis by reovirus cores in the presence of S30INT is the same as in the presence of S30C. However, the methylation of the de novo synthesized reo mRNA by the core-associated methylating enzyme(s) in vitro is inhibited by S30INT but not by S30C. The relevance of these phenomena to the inhibition of reovirus replication in interferon-treated cells remains to be established.
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PMID:Impairment of reovirus mRNA methylation in extracts of interferon-treated Ehrilich ascites tumor cells: further characteristics of the phenomenon. 55 82

Interferon production was induced in mouse Ehrlich ascites tumor cells by infection with Newcastle disease virus. The interferon produced was purified by precipitation with ammonium sulfate, chromatography on carboxymethyl-Sephadex, treatment with blue dextran and polyethylene glycol, gel filtration on Bio-Gel P-60 and Bio-Gel P-200, chromatography on phosphocellulose, isoelectric focusing, and chromatography on octyl-Sepharose. The specific activity of the product was 1.6 x 10(9) NIH mouse interferon reference standard units/mg of protein. Electrophoresis in polyacrylamide gels in the presence of sodium dodecyl sulfate indicated that the apparent molecular weight of the interferon-active material ranged from 25,000 to 35,000. As revealed by staining the gels with Coomassie brilliant blue, the interferon activity co-migrated with the major, broad protein band. Minor, stainable bands of proteins were free of interferon activity and their apparent molecular weight was smaller than 12,000.
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PMID:Purification of interferon from mouse Ehrlich ascites tumor cells. 56

We have determined the effect of sheep anti-mouse interferon globulin on the anti-tumor effects of poly I-C, statolon, tilorone, pyran copolymer and BCG in mice inoculated with Ehrlich ascites or L 1210 lymphoma cells. Whereas the anti-tumor effects of poly I-C and statolon were nulified when mice were injected with immunoglobulins, the anti-tumor effects of pyran copolymer and BCG were not modified by this treatment. We conclude that interferon mediates the anti-tumor activity of poly I-C and statolon in these experimental systems. It is suggested that anti-interferon serum provides a direct method of determining whether other biologic effects attributed to viruses, poly I-C, statolon, tilorone, pyran copolymer (and possibly other interferon inducers) are mediated or not by interferon.
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PMID:Role of endogenous interferon in the anti-tumor effect of poly I-C and statolon as demonstrated by the use of anti-mouse interferon serum. 56 32

Alcohol appears to exert a depressive effect on host immunity. Animal models useful in studying immune responsiveness in cancer research are discussed, which could be of value in studying the effect of alcoholism. Allogeneic tumor grafts are poorly rejected in immunosuppressed mice. Of the four major cellular elements of the immune system, the macrophage appears to have a critical role in immune surveillance. Several conditions occur which abrogate or restrict the tumoricidal activity of macrophages. Stress induced by physical restraint results in depressed macrophage activation. The tumoricidal activation induced in macrophages by interferon was markedly depressed in the presence of the corticosteroids, hydrocortisone, prednisone, and dexamethasone. In addition, prostaglandins (PGE1 and PGE2) also were found to decrease interferon activation of macrophages. Since immune deficiency is a trait of alcoholism and cancer, animal models with defined, measurable, immunological parameters would be useful in studying the effect of alcohol on cellular immunity.
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PMID:Animal models in cancer research which could be useful in studies of the effect of alcohol on cellular immunity. 57 62


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