Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbits immunized with interferon from mouse L cells for long periods of time produced interferon-neutralizing antibodies with titers from 1:80 to 1,2000. The anti-interferon sera also contained antibodies against antigens contaminating the interferon preparations such as albumin, bovine gamma-globulin, chicken albumin, extract from L cells, and Sindbis virus antigens. Some sera also displayed cytotoxic activity against cells of transplantable murine leukemia. These antibodies could be removed by specific absorption. Titers of antibodies neutralizing interferon were not correlated with the titers of antibodies against concomitant antigens. In hyperimmunized rabbits interferon-neutralizing antibodies persisted for long periods of time in spite of interrupting immunization.
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PMID:Biological activity of sera obtained by hyperimmunizing rabbits with interferon from mouse L cells. 44 43

In vitro production of interferon by blood leukocytes from patients with lymphosarcoma, lymphogranulomatosis, leukemia, cancer tumours, pneumonia, as well as by leukocytes of mice with Rauscher leukemia, and mice in the condition of hyporeactivity to interferon inducer was studied. Alongside with quantitative differences in interferon production, biological differences in the properties of interferons produced of normal and sick humans and animals were revealed. The biological differences consist in that the interferon produced by leukocytes from cancer and leukemia patients interacting with homologous cell culture is conducive to more rapid formation of resistance to the indicator virus than the interferon produced by normal leukocytes. Thus, resistance of the homologous cell culture to the infection with the indicator vesicular stomatitis virus developed within 1--2 hours after contact with leukocyte interferon from patients and only within 5--6 hours after contact with that of normal subjects. This finding is not specific for cancer and leukemia, as the same was observed with specimens from patients with pneumonia and from mice hyporeactive to interferon inducer. It is suggested that patients with cancer and leukemia have a state of interferon hyporeactivity.
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PMID:[Differences in the properties of the interferons produced by the leukocytes of healthy persons and of cancer and leukemia patients]. 50 7

The effect of mouse interferon (ITF) on the expression of Friend leukaemia virus (FLV) an on dimethyl sulphoxide (DMSO)-stimulated haemoglobin synthesis in Friend erythroleukaemic cells (FLC) was studied. Immunofluorescent staining was used to detect intracellular antigens, and incorporation of 3H-uridine into virions to detect extracellular virus release. Interferon markedly inhibited haemoglobin synthesis and FLV production, but enhanced accumulation of virus antigens in the cytoplasm; on the cell surface, however, FLV antigens were present to the same extent whether ITF was present or not. When ITF was removed, virus production rose and intracellular virus antigens fell to the levels of untreated controls.
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PMID:Production of Friend leukaemia antigens in chronically-infected cells treated with interferon. 56 23

Persistence of Sindbis virus (SV) was studied for 9 months in two lines of mouse cell cultures (BALB/C) in one of which the genome of endogenous ecotropic oncornaviruses was repressed. The other lines was exogenously infected at the level of plimary culture with Rauscher leukemia virus (RLV) and SV and showed gradual inhibition of oncornavirus functions. The presence of oncornavirus type C was not the necessary condition for the development of persistent SV infection, however it influenced the character of persistence. In both systems, sequential loss of the hemagglutinating and interferon-inducing activities, then infectivity of SV (61--82 days), and persistence of the noninfectious antigen of the arbovirus for 9 months were observed. The differences consisted in the time of appearance of homologous interference to SV: in the presence of oncornavirus earlier (40 days), under conditions of repressed oncornavirus genome later (179 days). Electron microscopic examinations showed that in the system infected with RLV and SV there occurred in the course of persistence a sharp activation of phagosome-lysosome complex accompanied by incorporation into phagocytolysomes of numerous intact and partially destroyed virions of SV and RLV and their release from cell with cytoplasmic fragments. Possible mechanisms of inhibition of functions of the oncogenic and infectious viruses in the reported model of mixed chronic infection are discussed.
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PMID:[Persistence of Sindbis virus in cultures either non-producing or irregularly producing oncornavirus]. 64 57

Mouse cells productively infected with Moloney murine leukemia virus were treated with interferon, and intracellular virus-specific RNA was studied by hybridization with complementary DNA. The steady-state concentration of virus-specific RNA in interferon-treated cells was somewhat greater than that in untreated cells, and the rates of virus-specific RNA synthesis were approximately equal in treated and untreated cells.
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PMID:Virus-specific RNA synthesis in interferon-treated mouse cells productively infected with Moloney murine leukemia virus. 69 Nov 18

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

With the object of examining the anti-tumour effect of exogenous interferon therapy in man a research programme has been initiated at the Karolinska Hospital. Established cell lines obtained from patients with Burkitt's and other types of lymphoma, leukaemia, osteosarcoma, mammary carcinoma and fibrosarcoma and from fibroblast cultures displayed a variable sensitivity to the cell multiplication inhibitory activity of interferon. All the monolayer cultures tested were found to be sensitive to interferon at concentrations between 10 and 300 units/ml. Some lymphoma cell lines were not sensitive to interferon even at concentrations as high as 10.000 units/ml, while others were sensitive at concentrations between 2 and 300 units/ml. The interferons tested appeared to show a degree of tissue specificity. Controlled studies in vivo are being performed on osteosarcoma, juvenile papilloma of the larynx, multiple myeloma and small-cell carcinoma of the lung. The clinical results of this research obtained to date, together with the results obtained in model experiments, would appear to warrant accelerated production of human interferon.
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PMID:Interferon therapy for neoplastic diseases in man in vitro and in vivo studies. 72 40

Normal subjects and patients with lymphoma or leukemia were tested for the levels of lymphocytes, E-rosette--forming T-cells, serum and vesicle fluid interferon, and specific in vitro proliferative response to varicella-zoster antigen after clinical varicella or herpes zoster illness. The effect of polyinosinic acid/polycytidilic acid on the immune response was also evaluated. The development of VZ specific cell-mediated response in normal subjects was characterized by intense proliferative activity eight to ten days after the onset of illness, with significant decline 70 to 80 days later. The responses in subjects with lymphoma or leukemia were much lower. Few subjects with chickenpox or zoster with lymphoma or leukemia died during the infection. Death was associated with significant depletion of E-rosette--forming T-cells, and grossly deficient specific cellular response to VZ antigen. Treatment with Poly IC frequently induced elevations in serum as well as vesicle fluid interferon levels, and increased the proliferative activity of lymphocytes against VZ antigen.
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PMID:Cell-mediated immunity to varicella-zoster virus infection in subjects with lymphoma or leukemia. 76 11

The prolonged adminstration of rabbit anti-mouse L cell interferon globulin had a marked potentiating effect on Rauscher Murine Leukemia Virus (MuLV-R) infection in BALB/c mice, as shown by spleen size. Normal rabbit globulin had a lesser, but still significant, augmenting effect on splenic enlargement. It was possible to discriminate quantitatively between the non-specific enhancement of splenomegaly in MuLV-R infected mice due to antigenic stimulation with normal rabbit globulin and the effects due to elimination of endogenous interferon by specific antibodies. The difference in the spleen-enlarging activity between the anti-interferon IgG and normal rabbit IgG was found to be maximal 3-4 weeks after infection when potent, diluted anti-interferon IgG (58 microgram protein per dose) was used. It would appear that the endogenous interferon, even prodcued in undetectable amounts, plays an essential role in controlling infection with an oncogenic virus.
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PMID:Enchancement of leukemogenesis in mice after prolonged administration of anti-interferon or normal rabbit globulin. 92 45

The essential role of Rauscher leukemia virus (RLV) multiplication in viral-chemical co-carcinogenesis was investigated by the use of ethidium bromide (EtBr) as an inhibitor of viral complementary DNA (cDNA) integration in the host genome. EtBr inhibited co-carcinogenic transformation when present at the time of RLV inoculation but was ineffective when added to preinfected cells. Inhibitors of protein synthesis, puromycin and cyclohexamide also inhibited co-carcinogenic transformation of chronically infected cells. Purified rat interferon used at a concentration which inhibited 85% of RLV production did not modify the course of co-carcinogenic transformation. The implications of these observations in terms of the possible role of the virus-specific protein (s) in the co-carcinogenic process are discussed.
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PMID:Chemical-viral co-carcinogenesis: requirement for leukemia virus expression in accelerated transformation. 99 12


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