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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Susceptibility of BALB/c mice to infection with Moloney sarcoma virus (MSV) and to Herpes simplex virus type 2 (HSV-2) was considerably increased by administration of sheep anti-mouse interferon (anti-IF) serum. The regression of the MSV-induced tumors was inhibited when the weanling (three-to-four-week-old) mice were injected with the anti-IF serum. Using the anti-IF serum it has been found that the antagonism between HSV-2 and Rauscher leukemia virus in the mouse is not mediated by interferon. It is suggested that interferon is an important factor controlling growth of virus and/or virus induced tumor cells in the mouse before it develops a strong immunological response.
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PMID:Application of antisera to interferon in studying oncogenic viruses. 21 9

Different preparations of human interferon inhibit virus production in human cells chronically infected by a variety of type-C xenotropic viruses. Some of these viruses have been incriminated in the development of leukemia in primates. The characteristics of blocking of viral multiplication are similar to those described for the effect of mouse interferon on ecotropic viruses. The amount of free virus in culture supernatants is strongly decreased while intracellular protein p30 stays unchanged or is slightly increased. On the other hand, the inhibitory effect is reversible. The withdrawal of interferon results in a rapid increase in virus production as detectable in supernatant fluids. In the light of these results it is suggested that human interferon might be useful in the treatment of some blood malignancies suspected of being related to infection with xenotropic type-C viruses.
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PMID:Effect of interferon on chronic infection of human cells by xenotropic type-C viruses. 22 93

NIH 3T3 mouse cells were infected at very high multiplicity with murine sarcoma/leukaemia virus (MSV/MLV) and then cloned. All of the 48 clones obtained were morphologically transformed, all but one showed anchorage-independence of growth, typical of MSV-transformed NIH 3T3 cells and most (91%) produced MSV/MLV. When cells which had been pre-treated with 10(4) units/ml of purified interferon (IF) were infected under the same conditions and then cloned in the presence of the same amount of IF, only 6 of a total of 63 clones were morphologically transformed. All but these 6 showed a degree of anchorage-independence typical of the uninfected parental cells and very few (2.4%) produced virus. Furthermore, the MSV genome could not be rescued in any of the 23 clones tested and only 1 out of 10 clones produced tumours. The properties of these clones remained stable over a period of 10 to 20 passages in the absence of interferon. We conclude that interferon can irreversibly block an early step in the MSV/MLV infectious process.
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PMID:An interferon-sensitive early step in the establishment of infection of murine cells by murine sarcoma/leukaemia virus. 22 16

Expression of simian papovavirus 40 (SV40) T-antigen following in vitro infection was studied in skin fibroblasts from patients with Down syndrome (DS) and their parents to determine whether the increased susceptibility to SV40 infection reflected the cytogenetic defect or the leukemia risk associated with this syndrome. As a group, fibroblasts from patients with DS showed elevated T-antigen expression 72 hrs after infection compared to that of a healthy control population. However, among 24 patients tested, the cell lines of only 11 showed statistically significant increases in T-antigen expression. A cell line from a patient with concurrent DS and acute myelogenous leukemia had a normal value. T-antigen expression did not correlate with the percentage of cells trisomic for chromosome 21 in 18 cell lines examined or with the number of copies of this chromosome in disomic and trisomic cell strains cloned from three mosaic patients.Collectively, cell lines from parents of trisomy 21 patients also showed increased susceptibility to SV40 infection; however, in five families tested, a consistent pattern of genetic transmission of elevated T-antigen expression from parent to offspring was not observed. Q-banding of cell lines in one family showed that elevated T-antigen expression is not a marker of parental nondisjunction. Variation in susceptibility to human interferon, an antiviral agent, did not account for variation in T-antigen levels among these cell lines. Thus, the abnormalities of T-antigen expression in DS appear independent of the hyperdiploid state and are not a sensitive indicator of cancer risk.
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PMID:SV40 T-antigen expression in cultured fibroblasts from patients with Down syndrome and their parents. 22 51

Constant intracellular concentrations of both adenosine 3',5'-cyclic-monophosphate (cyclic AMP) and guanosine 3',5'-cyclic-monophosphate (cyclic GMP) were obtained when leukemia L1210 cells were cultivated under steady-state conditions in the chemostat. In this sensitive and controlled system addition of mouse interferon resulted in a rapid (5-10 min) increase in the intracellular concentration of cyclic GMP, which preceded by several hours an increase in the intracellular concentration of cyclic AMP. In contrast to the effect of interferon, addition of prostaglandin E1 induced a rapid increase in the intracellular concentration of cyclic AMP without markedly affecting the intracellular concentration of cyclic GMP. It is suggested that the rapid effect of interferon on cyclic GMP plays a role in mediating some of the effects of interferon on cells.
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PMID:Effect of interferon on concentrations of cyclic nucleotides in cultured cells. 22 87

In cultures of Ly cells treated with 10 or 30 reference units/ml of mouse interferon there was a 30 to 200 times reduction in the production of infectious vesicular stomatitis virus (VSV); virus particle production, as measured by VSV particle associated virus RNA, virus protein, and virus transcriptase, was inhibited by, at most, six times. These results suggested that interferon-treated cells produce VSV particles with low infectivity and resemble the findings in interferon-treated cells infected with murine leukaemia viruses.
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PMID:Production of vesicular stomatitis virus with low infectivity by interferon-treated cells. 22 98

SN11841 [4'-(9-acridinylamino)-methanesulfon-m-aniside] is an antitumor compound discovered by B.F. Cain. The LD50 for BALB/c mice with single intraperitoneal dosage is approximately 25 mg/kg. RLV-(Rauscher leukemia virus)-induced splenomegaly, a disease indicator in BALB/c mice, is inhibited at SN11841 doses not causing acute mortality. The life span of RLV-infected mice increases at some SN11841 doses. SN11841 does not have direct, or virolytic effects on RLV under conditions approximating those of antiviral effectiveness. SN11841 is cytotoxic for cells in tissue culture, as measured by inhibition of growth rate or vital dye uptake. At nontoxic concentrations SN11841 has no effect on RLV infectivity for murine cells, as determined by XC-cell induced syncytium formation. SN11841 has antiviral activity against vaccinia virus in tissue culture but is inactive against herpes simplex (Type 1), vesicular stomatitis, encephalomyocarditis, or reoviruses. SN11841 apparently does not act by inducing interferon. SN11841 is chemically labile, particularly in the presence of sulfhydryl compounds, but the degradation products resulting from prolonged storage in media are neither cytotoxic nor antiviral.
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PMID:Antiviral activities of 4'-(9-acridinylamino)-methanesulfon-M-aniside (SN11841). 28 Jan 45

Leucocyte interferon production in vitro and circulating interferon levels were studied in healthy subjects and in 80 patients with acute or chronic leukaemia. Circulating interferon was not found in either group. Interferon synthesis in response to a virus was normal in patients with acute leukaemia and appeared to be enhanced in some. In chronic leukaemia reduced levels were common particularly in CLL, in which condition normal results were rarely found; lymphocyte transformation to PHA was also depressed in this group. No clinical or haematological correlation with the interferon levels was found and no consistent effect of treatment was shown. The possible factors which could account for these findings and their significance in relation to pathogenesis and treatment of leukaemia are discussed.
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PMID:Interferon production in leukaemia. 28 Mar 60

Host defense mechanisms against cancer depend on an intact cellular immunity system. Immunosurveillance depends on thymus lymphocytes which, when sensitized, form lymphokines. One of the important lymphokines produced by T-lymphocytes is called interferon, well known for its antiviral effects. Recent experimental evidence points also to the potential effectiveness of interferon against malignancies. Interferon and interferon-inducers have been found to alter the course of solid tumors, leukemia, sarcomas and lymphomas in experimental animals, possibly by stimulating the reticuloendothelial system to produce tumor rejection or by altering the surface of cells to change tumor and host reactions.
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PMID:Tumor immunology and interferon. 36 39

Mice sensitized with either BCG or cell-wall skeleton of BCG (BCG-CWS) produced interferon in blood after stimulation with specific antigen, purified protein derivative of tuberculin (PPD). Both BCG-infected normal (C57BL/6) and thymic nude (BALB/c, nu/nu) mice showed enhanced activity to produce interferon by stimulation with E. coli endotoxin. However, detectable interferon was not produced in athymic nude mice sensitized with BCG or BCG-CWS by stimulation with PPD. Immune-induced interferon (I-IF) produced by BCG-CWS and PPD in mice was different in biological and physicochemical properties from virus-induced interferon. I-IF showed about 100 times more potent L-cell growth inhibitory activity than virus-induced L-cell interferon (L-IF). Both I-IF and L-IF showed macrophage-activating activity, which renders resting macrphages cytotoxic to L1210 leukemia cells. Antiviral and macrophage-activating activity of interferon preparation was not separated physicochemically in this study.
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PMID:Properties of interferon induced by purified protein derivative of tuberculin in mice sensitized with BCG or cell-wall skeleton of BCG. 38 26


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