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)

RBL-5 leukemia induced by Rauscher murine leukemia virus (R-MuLV) carried in the ascites form in C57BL/6 mice was cultivated in vitro and passaged continuously. Both low- and high-passage cells released the same level of murine leukemia virus, as detected by the XC plaque assay. Membrane antigens of the cultivated cells were also detected by the indirect immunofluorescence assay. Both low- and high-passage cells showed the same activity of antigen detectable by anti-R-MuLV serum, whereas only the high-passage cells reacted strongly against a syngeneic antiserum to RBL-5 crude membrane (CM). The oncogenicity of the low and high passages of the cultivated cells was compared with the ascites cells. The results indicated that the oncogenic potential of the cells gradually decreased during in vitro passage. The accumulation or retention of CM antigen on the membrane of the high-passage cells suggested that their decreased oncogenic potential might be due to increased immunogenicity and/or immunosensitivity. This strengthened the hypothesis that the cellular transplantation antigens are not identical to type C viral antigens, since the R-MuLV antigens were not altered during passage in vitro.
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PMID:Properties of RBL-5 leukemia cells cultivated in vitro. 86 45

Defective Friend spleen focus-forming virus (SFFV) is able to interfere with the ability of its naturally occurring leukemia-inducing helper virus (LLV-F) to induce XC plaque formation in several different strains of mouse embryo cells. This interference has been observed by using two different SFFV preparations, one contained in an NB-tropic stock of Friend virus (FV) complex, and the second present in a C57BL-adapted strain of FV complex containing an associated B-tropic LLV-F helper. The LLV-F in NB-tropic FV complex effectively induced XC plaques in C57BL/6 (Fv-1(bb); Fv-2(rr)) mouse embryo fibroblasts (MEF) only in the absence of coinfecting SFFV, indicating that Fv-2-associated resistance to SFFV-induced focus formation in vivo does not necessarily extend to the restriction of SFFV function(s) in vitro (i.e., in Fv-2(rr) C57BL MEF). SFFV interference appears to be an intracellular event since LLV-F can adsorb onto, penetrate, and rescue defective murine sarcoma virus (MSV) from transformed 3T3FL S(+)L(-) cells with equal efficiency in the presence and absence of SFFV. However, significantly fewer LLV-infected S(+)L(-) cells released LLV-F progeny if SFFV was present. These observations suggest that Friend SFFV may be classified as a defective, interfering (DI) particle. Further support for this conclusion has come from studies designed to investigate two physical properties of defective SFFV particles. SFFV layered onto a 0 to 20% sucrose sedimentation gradient was recovered as a symmetrical band of virus that sedimented more slowly than standard LLV-F particles. Pooled SFFV-containing gradient samples contained visualizable type C virus particles and occasionally small amounts of detectable LLV-F. In an attempt to determine the buoyant density of sedimentation gradient-purified SFFV, pooled SFFV samples were layered onto a 25 to 50% sucrose equilibrium density gradient and were centrifuged to equilibrium. Greater than 50% of the infectious SFFV originally layered onto this gradient was recovered and seen as a narrow symmetrical band with peak SFFV infectivity at a sucrose density of 1.14 g/ml. The observed difference between SFFV and LLV-F buoyant densities appears to be related to an inherent physical property of each virus. Mixtures of these two viruses express the buoyant density of that virus population which is in excess in fabricated FV complexes probably due to the formation of SFFV-LLV aggregates. Finally, gradient-purified SFFV failed to induce XC plaques in MEF and did not function to rescue MSV as expected since SFFV itself is replication defective.
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PMID:Defective Friend spleen focus-forming virus: interfering properties and isolation free from standard leukemia-inducing helper virus. 90 28

The correlation of murine leukemia virus (MuLV) infection and leukemogenesis was examined by XC plaque assay in W/F rats neonatally infected with the rat-adapted Gross virus (RAGV). Thymic lymphomas developed in 100% of infected rats, with a mean latent period of 64 days. The virus infectivity was first detected in the thymus as early as 15 days after the virus infection; the titer steadily increased thereafter until the development of thymic lymphoma. No other tissues of virus-infected rats showed virus infectivity until the development of localized thymic lymphoma, though sera of a few rats showed low infectivity titers. In rats with generalized leukemia, however, high titers were detected in the sera and leukemic tissues. In untreated controls, all tissues tested invariably showed negative titers for MuLV infectivity at any age up to 7 months after birth. The results indicated that those tissue sites were common to both RAGV infectivity and the leukemogenic process, with the primary involvement of the thymus, and that the appearance of RAGV infectivity in various tissues represented the expression of the oncogenic genome of RAGV.
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PMID:Type C RNA viruses and leukemogenesis: association of Gross strain of murine leukemia virus infection and leukemogenesis in rats. 99 3

A fraction of the unintegrated viral DNA that appears early after infection of mouse cells by Moloney leukemia virus is infectious. The infectivity could be deomonstrated by an XC plaque assay of the cells exposed to DNA co-precipitated with calcium phosphate. The number of plaques deriving from closed-circular, supercoiled DNA was proportional to the concentration of added DNA, indicating that a single DNA molecule of about 5.5 X 10(6) daltons carries all the viral information. Nonsupercoiled viral DNA is also infectious; these molecules appear to be largely double-stranded and 5 to 6 X 10(6) dalthons in mass.
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PMID:Infectious viral DNA of murine leukemia virus. 106 Oct 80

S-Adenosylhomocysteine hydrolase (AdoHcy-nase) is a key enzyme in transmethylation reactions. The objective of the present study was to examine the potential antiretroviral activities of novel mechanism-based irreversible AdoHcy-nase inhibitors. (Z)-4',5'-didehydro-5'-deoxy-5'-fluoroadenosine (ZDDFA), (E)-4',5'-didehydro-5'-deoxy-5'-fluoroadenosine (EDDFA), (Z)-4',5'-didehydro-5'-deoxy-5'-chloroadenosine (ZDDCA) and 5'-deoxy-5'-acetylenic adenosine (DAA) inhibited AdoHcy-nase activity with Ki values of 0.55, 1.04, greater than 10.0 and 3.30 microM, respectively. These four compounds were tested for antiviral activity in vitro against Moloney leukemia virus (MoLV) in the XC-plaque assay. MoLV replication in murine fibroblasts (SC-1) was inhibited by ZDDFA, EDDFA and DAA with IC50 values of 0.05, 0.25 and 3.30 micrograms/ml, respectively. ZDDCA did not inhibit MoLV infection at the concentrations tested. Antiviral activity correlated with the ability of the individual compounds to maintain sustained elevations in intracellular S-adenosylhomocysteine (AdoHcy) concentrations in the SC-1 cells. ZDDFA, the most potent inhibitor of AdoHcy-nase and MoLV was also the most active in maintaining sustained elevations in intracellular AdoHcy levels. The antiviral activity of ZDDFA was also examined in murine C3H1OT1/2 fibroblasts which constitutively produce MoLV. Pretreatment with ZDDFA (1.0 microgram/ml) for 24 hr inhibited virus production by 88%. Similar to the SC-1 cells, and concomitant with enzyme inhibition, there was a 300-fold increase in AdoHcy levels in ZDDFA (1.0 microgram/ml) treated C3H1OT1/2 cells. Incorporation of a [3H]methyl group from tritiated S-adenosylmethionine into total RNA in C3H1OT1/2 cells was inhibited by ZDDFA without affecting cell viability. These results suggest that mechanism-based inhibitors of AdoHcy-nase, such as ZDDFA, may have potential as antiretroviral agents.
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PMID:Antiretroviral activity of mechanism-based irreversible inhibitors of S-adenosylhomocysteine hydrolase. 137 45

A system for evaluating the activity of antiviral agents against Rauscher murine leukemia virus (R-MuLV) has been developed using an enzyme linked immunosorbent assay technique. The activity of various antiviral compounds demonstrated in this assay system has been compared to their activity in the UV-XC plaque reduction assay, which has been used historically for evaluating anti-R-MuLV compounds. The assay is based upon detection of R-MuLV encoded p30 protein production in virus infected murine cells. The assay reagents are readily available and the assay system is amenable to automated data collection systems. Cytotoxicity evaluations are conducted in parallel to the Rauscher MuLV ELISA assay in order to assess drug-induced reductions in cell viability. Cytotoxicity evaluations are important to interpretation of the ELISA results since reductions in cell viability reduce viral protein production which would indicate an antiviral drug effect. This system is less sensitive than the classical UV-XC plaque reduction assay; however, it does offer an alternative to the time-consuming and labor-intensive plaque assay.
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PMID:An ELISA system for evaluating antiretroviral activity against Rauscher murine leukemia virus. 141 8

From a plaque biopsy of a patient with mycosis fungoides, two different continuous cell lines were established by including both IL-2 and IL-4 in the culture medium. Both continuous cell lines appeared with characteristic chromosome markers after approximately 40 cell population doublings. The initial karyotype recognized in T cells from the skin biopsy was 46,XY and the karyotypes of the continuous cell strains were 46,XY, -18, + i(18q) and another with multiple chromosome aberrations as described in Sezary T-cell leukemia. Phenotyping with monoclonal antibodies and T-cell receptor analysis indicates that the latter cell strain represents a minority of T-cells in the plaque. Due to its many chromosomal aberrations it probably represents the malignant cell, which may be a central cell in the immune stimulation taking place in the skin.
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PMID:Establishment of two continuous T-cell strains from a single plaque of a patient with mycosis fungoides. 158 90

It was previously shown that spleen cells from endogenous ecotropic murine leukemia virus emv-14+ AKXL-5 mice fail to stimulate an anti-AKR/Gross virus cytolytic T-lymphocyte (CTL) response in a mixed lymphocyte culture with primed C57BL/6 responder spleen cells, whereas spleen cells from AKXL strains carrying the very similar emv-11 provirus do stimulate a response (Green and Graziano, Immunogenetics 23:106-110, 1986). We wished to determine whether the lack of response with AKXL-5 spleen cells was at the level of recognition between effector cell and target cell and whether the relevant mutation was within the emv-14 provirus. It is shown here that EMV-negative SC-1 fibroblast cells transfected with the major histocompatibility complex class I Kb gene and infected with virus isolated from the AKXL-5 strain (SC.Kb/5 cells) were not lysed by H-2b-restricted anti-AKR/Gross virus CTL. SC.Kb cells infected with virus isolated from emv-11+ strains, however, were efficiently lysed by anti-AKR/Gross virus CTL, indicating that there is nothing intrinsic to EMV-infected SC.Kb cells that would prevent them from being recognized and lysed efficiently by anti-AKR/Gross virus CTL. Analysis of virus expression for the infected SC.Kb cells by XC plaque assay and by flow cytometry indicated that emv-14 virus expression for SC.Kb/5 cells was not significantly different from that for emv-11-containing SC.Kb/9 or SC.Kb/21 cells. These data show that the mutation responsible for the lack of CTL recognition and lysis is at the level of recognition between target cell and effector cell. Furthermore, these data strongly suggest that the mutation is within the emv-14 genome. Flow cytometry experiments with monoclonal antibodies against a number of viral determinants indicated that there was no gross mutation detectable in the viral determinants analyzed. The data suggest that the relevant mutation may be a point mutation or a small insertion or deletion within a coding sequence that is critical for CTL recognition.
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PMID:Mechanism of escape of endogenous murine leukemia virus emv-14 from recognition by anti-AKR/Gross virus cytolytic T lymphocytes. 169 45

Various samples from lymphoproliferative diseases in the skin were analyzed by Southern blotting technique with probes from the T cell receptor gene, immunoglobulin genes, and human T cell leukemia virus-I genome. Samples were taken from 10 mycosis fungoides (MF) patients, 1 parapsoriasis en plaque patient, 10 Adult T cell leukemia/lymphoma (ATL) patients, 1 cutaneous T cell lymphoma (CTCL) patient, 4 lymphomatoid papulosis (LP) patients, 4 B cell lymphoma patients, and 2 actinic reticuloid (AR) patients. In MF, the monoclonality of the T cells became detectable first in the skin when plaques develop to tumors then in lymph nodes, and finally in the blood lymphocytes, indicating this disease develops from local (skin) malignancy to systemic malignancy. In parapsoriasis en plaque, no monoclonality was detected in any sample. We could distinguish cutaneous ATL from the carrier state by detecting the T cell monoclonality and HTLV-I integration with these probes. One patient with CTCL showed detectable T cell monoclonality; 1 out of 4 patients with LP did the same. Four samples from patients with B cell lymphoma revealed detectable monoclonal rearrangement of immunoglobulin heavy and light chain genes. In AR, no monoclonality was detected in any sample. From these data, we conclude that DNA analysis is useful in determining the monoclonality, cell origin, and distribution of monoclonal cells from skin samples.
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PMID:Characterization of the lymphoproliferative diseases in the skin by DNA analysis. 180 May 28

The effect of large granular lymphocyte leukemia on B lymphocyte function was studied by determining the number of plaques formed in an in vitro hemolytic plaque assay. Leukemia cells inhibited plaque formation by normal splenic lymphocytes in a logarithmic, dose-dependent manner. At the highest leukemia cell concentrations, spleen cell suspensions made 50% fewer plaques. Plaque forming responses were very sensitive to duration of preincubation time in all assays. The number of plaques formed decreased markedly if incubated 2 hr before the assay was performed. Incubation of the cells at 56 degrees C for 8 min did not alter the inhibitory activity but pretreatment with 0.01% trypsin did. Supernatant fluids from leukemia cell suspensions did not inhibit plaque formation. These data suggest that diffuse infiltration of lymphoid tissues by leukemia cells may interfere with some normal lymphocyte functions. Although leukemia cells inhibited splenic B lymphocyte function, leukemic rats did not have hypogammaglobulinemia.
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PMID:Inhibition of in vitro plaque formation by large granular lymphocyte leukemia cells from F344 rats. 196 81


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