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)

Tumours developed in chronic infection lasting for 150--180 days in 39 (60%) of 65 mice infected with strain L2 of herpes simplex virus (HSV) type 1 and in 12 (20%) of 60 mice infected with strain 333 of HSV type 2. Similar results were obtained in 150 immunosuppressed mice chronically infected with HSV types 1 and 2. Pathomorphologically, the neoplasias in the first group (strain L2) were similar to adenocarcinoma and malignant lymphoma and in the second (strain 333) to lymphoma and angio- or fibrosarcoma. The respective HSV strains were isolated by cocultivation of blood leukocytes from chronically infected animals and cultures of the tumour cells with human embryo fibroblasts (HEF). HSV and Gross murine leukaemia virus antigens were detected in tumour cells by immunofluorescence and radioimmunoassay, respectively, and HSV antigen by immunofluorescence also in cultures of tumour cells and in cells of the brains, spinal cords, livers and spleens of the animals. HSV antibody was demonstrable in the blood serum from chronically infected tumour-bearing mice in a titre of 32.
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PMID:Development of tumours in mice chronically infected with herpes simplex virus. 4 95

In view of the marked antitumor activity of 3-deazauridine, the synthesis of 4-(beta-D-ribofuranosyl)-1,3-dihydroxybenzene (1,3-dideazauridine) and its dibenzyl derivative was carried out. 4-Bromo-1,3-dihydroxybenzene was converted to its dibenzyl derivative, which, upon reaction with n-butyllithium followed by treatment with anhydrous cadmium chloride, gave bis(1,3-dibenzyloxyphenyl-4)cadmium. Condensation of this intermediate with 2,3,5-tri-O-benzoyl-D-ribofuranosyl chloride in refluxing toluene, and subsequent removal of the protecting benzoyl groups, afforded 4-(beta-D-ribofuranosyl)-1,3-dibenzyloxybenzene which, upon catalytic hydrogenation over Pd/C, furnished the desired 4-(beta-D-ribofuranosyl)-1,3-dihydroxybenzene. The beta configuration at the anomeric center was established by NMR and hydrogen bonding studies. 4-(Beta-D-ribofuranosyl)-1,3-dibenzyloxybenzene inhibited the growth of leukemia L1210 cells by 50% at 7 x 10(-6) M, and that of mammary carcinoma TA3 cells at 5 x 10(-5) M. Dideazauridine itself was less active, inhibiting the leukemia L1210 but not the TA3 cells at 1 x 10(-4) M, but the compound was significantly active against herpes simplex (type I) virus in vitro.
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PMID:Synthesis and biological activity of 4-beta-Iribofuranosyl-1,3-dihydroxybenzene ("1,3-dideazauridine"). 16 82

The direct acylation of 2,2'-anhydro-1(beta-D-arabinofuranosyl)cytosine hydrochloride (cycloC) with a homologous series of saturated and unsaturated acyl chlorides in dimethylacetamide has been investigated. Such acylation reactions have made available a considerable number of 3',5'-diesters of cycloC that have been examined for biological activities. The compounds all show cytotoxicity against HeLa cells in tissue culture, and with the exception of the highly insoluble long-chain diesters (C16--C22), show pronounced activity against vaccinia and Herpes simplex viruses. Against L1210 leukemia in mice the compounds show varied activities, the C12--C14 saturated diesters and the C18--C22 unsaturated diesters being highly effective. Other diesters, varying by only a few methylene groups, show dramatically different results.
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PMID:Reactions of 2-acyloxyisobutyryl halides with nucleosides. 7. Synthesis and biological evaluation of some 2,2'-anhydro-1(3',5'-di-O-acyl-beta-D-arabinofuranosyl)cytosine hydrochlorides. 17 72

In AKR mouse cells chronically infected with a murine leukemia virus, treatment with interferon for nine days resulted in sustained inhibition of extracellular production of murine leukemia virus but no inhibition of viral intracellular p30 antigen or of reverse transcriptase. Removal of interferon resulted in rapid reversal of these effects. Interferon-treated mouse L-cells were infected with high multiplicities of vesicular stomatitis virus or herpes simplex virus type 1. Infectious virus and intracellular viral antigen were rapidly eliminated from the interferon-treated cultures infected with herpes simplex virus. In cultures infected with vesicular stomatitis virus, titers of virus remained low in interferon-treated cells, but after about two weeks they rose rapidly and the cultures were destroyed. If treatment with interferon was reinstituted as late as nine days after primary infection, infectious vesicular stomatitis virus was eliminated, and there was no evidence for survival of the viral genome in these cultures. In the cultures infected with murine leukemia virus, inhibition of production of virus by treatment with interferon was possible, but the viral genome was not eliminated. In cells acutely infected with vesicular stomatitis virus or herpes simplex virus, however, the viral genomes were apparently eliminated from cultures treated with interferon.
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PMID:Persistence of the viral genome in interferon-treated cells infected with oncogneic or nononcogenic viruses. 18 Feb 9

The interaction of endogenous type C viruses with superinfecting herpes simplex virus type 2 (HSV-2) was investigated in two murine cell lines. Replication of HSV-2 was suboptimal in random-bred Swiss/3T3A cells and, in initial experiments, infection with a low virus-to-cell ratio resulted in carrier cultures with enhanced murine leukemia virus (MuLV) p30 expression. Immunofluorescence tests with Swiss/3T3A cells productively infected with HSV-2 also showed HSV-associated cytoplasmic antigens and enhanced MuLV p30 expression when compared with uninfected controls. Inactivation of HSV-2 with UV light did not abolish this reaction, although the number of cells expressing p30 was reduced. HSV-2 replicated more efficiently in a line of NIH Swiss cells (N c1 A c1 10). These cells are not readily inducible for type C expression by conventional methods; however, untreated and UV-inactivated HSV-2 induced both HSV-2-associated antigens and MuLV p30 in these cells. Although the Birch strain of human cytomegalovirus induced MuLV p30, neither mouse cytomegalovirus nor vesicular stomatitis virus induced MuLV p30 in either cell line.
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PMID:Induction of murine p30 by superinfecting herpesviruses. 18 96

During the period of three years ((1972-1974), serum samples from 60 patients (children and adolescents) with lympho-hematopoietic system diseases were examined for antibodies to all four human herpesviruses. Among these were 26 active Hodgkin's disease (AHD) patients and 6 HD patients with a minimum five years' remission. Simultaneously matched controls (age, sex) of AHD patients were examined. Antibody levels against the viral capsid antigen of Epstein-Barr virus (EBV/VCA) in AHD patients were significantly higher, with overrepresentation of higher titres (greater than or equal to 1:160), than in matched controls. The lowest EBV/VCA antibody titres were in the leukemia-non-Hodgkin's lymphoma patients. We could not prove any significant relationship between cytomegalovirus or herpes simplex virus type 1 antibody titres and AHD or any other disease of lympho-hematopoietic system. The varicella-zoster virus antibody titres in AHD patients were significantly higher than in matched controls. No significant differences in antibodies against EBV/VCA and the other human herpes viruses between the evolution and remission period of AHD patients could be detected. No differences in EBV/VCA antibody titres were observed between the healthy school-children aged 10 to 15 years who were and who were not in contact with a HD patient.
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PMID:Herpesvirus group antibodies in children with Hodgkin's disease. 19 63

The ability of leukemic leukocytes to support the replication of herpes simplex virus (HSV) was studied. Mononuclear leukocytes (MNL) from the peripheral blood of patients with a variety of lymphoid leukemias were isolated on Ficoll-Hypaque gradients and infected with HSV at a multiplicity of infection of 5 to 10. No virus growth was detected in cells from patients with chronic lymphocytic leukemia (9), acute lymphocytic leukemia (1), or lymphosarcoma cell leukemia (2), HSV replication did occur in hairy cell leukemic MNL from all of 4 patients studied. Maximal titers of 10(3.7) to 10(4.7) PFU/ml occurred 1 to 7 days after incubation. By electron microscopy, herpesvirus particles were seen in the nuclei of these infected cells after 3 days of culture, but none was seen in the cells not exposed to virus. Fluorescent antibody examination confirmed the presence of HSV antigens in the nuclei of infected hairy cells. No difference in the adsorption or penetration of the virus was found with the various MNL studied. Productive infection of the cells thus appeared to depend on the ability of the leukocyte ;o support a later stage of infection, either uncoating or replication of the virus.
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PMID:Replication of type I herpes simplex virus in primary cultures of hairy cell leukemic leukocytes. 20 67

Immune adherence hemagglutination was compared with the complement fixation test as a means of measuring antibodies to varicella-zoster virus. Analysis of acute- and convalescent-phase sera from patients infected with varicella-zoster or with herpes simplex virus showed the immune adherence hemagglutination test to be more sensitive than the complement fixation test, and greater cross-reactivity between the two viruses appeared to be associated with the increased sensitivity. The two assay methods were used to measure antibodies to varicella-zoster virus in 265 sera obtained from patients of different ages as well as sera from 26 patients with leukemia. There were 35 cases where antibodies were detected by immune adherence hemagglutination but not by complement fixation, whereas in five cases the converse was found. Our findings support the contention that immune adherence hemagglutination is the method of choice for detecting antibodies to varicella-zoster virus.
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PMID:Quantitation of antibodies to varicella-zoster virus by immune adherence hemagglutination. 20 4

Mouse cells (line N cIA cl10) contain 1.2-2.5 ng murine leukaemia virus (MuLV) p30 antigen/mg of protein; this amount of antigen is measurable by competition radioimmunoassay (RIA) but is not detectable by indirect immunofluorescence (IF). Infection of N cIA cl10 cells with herpes simplex virus type 2 (HSV-2) induces expression of MuLV p30. Induction by HSV-2 does not require either cell or virus DNA synthesis and is optimal 8 h post infection when cells at 50-70% confluence are infected at a multiplicity of infection (MOI) of 5-8 PFU/cell. At an MOI of 2.5, 70-80% of the cells express HSV antigens while none of the cells express p30; at an MOI of 5.0, 70-80% of the cells express HSV antigens but 55% of the cells express p30. Using the conditions reported in this paper for preparation of competing antigen, induction of p30 by HSV-2 (strain 333) infection is not measurable by competition RIA.
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PMID:Conditions required for induction of murine p30 by herpes simplex virus. 21 Jan 28

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


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