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)

The gibbon ape leukemia virus (GaLVSF)-infected T cell line, MLA 144, was established from the lymphoma of a gibbon ape. The cell line constitutively expresses IL-2 and its receptor, implying that an autocrine mechanism could be responsible for or contribute toward its growth. To explore the mechanism of constitutive IL-2 expression in MLA 144, we have isolated and characterized cosmid clones representing a normal and a doubly inserted IL-2 allele in this cell line. The map of the normal MLA 144 IL-2 allele closely resembles that of the normal human IL-2 gene. The abnormal allele contains a 3' insertion that is a GaLVSF provirus with two long terminal repeats (LTR) and an internal 3.25 kb deletion. At the 5' end of the abnormal allele is a second insertion that DNA sequencing showed to be an isolated GaLVSF LTR with a transcriptional orientation opposing that of the IL-2 gene. We demonstrate by Northern blotting analysis that the vast majority of transcripts are from the abnormal allele, implying that one or both retroviral insertions are responsible for constitutive expression of the allele.
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PMID:Retroviral activation of interleukin 2 gene in a gibbon ape T cell lymphoma line. 302 92

Gibbon ape leukemia viruses (GALV) are a group of retroviruses which have been associated with hematopoietic neoplasms in primates. Two of the viruses, GALV-SEATO and GALV-San Francisco (GALV-SF), are associated with myeloid and lymphocytic leukemias, respectively, in apes. Using an assay based on the transient expression of the bacterial gene chloramphenicol acetyltransferase (CAT), we examined the transcriptional activity of GALV-SEATO and GALV-SF. The results suggest that high level expression of GALV is due primarily to cis-acting enhancer sequences. Sequence delineation analysis of GALV-SEATO showed the GALV-SEATO enhancer sequences to be located within a 45-bp tandem repeat in GALV-SEATO. GALV-SF, which has two- to fivefold lower transcriptional activity, contains only a single copy of the 45-bp element with 6-bp differences from those in the GALV-SEATO enhancer element. This 45-bp element is highly homologous to sequences within the LTRs of several murine leukemia viruses but has not been examined for enhancer function in these retroviruses. Expression of GALV was not restricted to hematopoietic cells but was extraordinarily high in MLA 144 cells, a gibbon ape T-cell line known to be infected with GALV-SF. However, expression of constructs containing the CAT gene directed by GALV-SEATO LTR sequences was similar in uninfected and GALV-infected fibroblasts, indicating the lack of virally encoded or virally induced trans-activating factors capable of increasing expression in these cells.
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PMID:Cis-acting transcriptional regulatory sequences in the gibbon ape leukemia virus (GALV) long terminal repeat. 302 59

The gibbon ape leukemia virus (GALV)-infected T-cell line, MLA 144, constitutively makes the lymphokine, interleukin 2 (IL 2), without stimulation by antigen or mitogen. This line contains two GALV insertions in the IL-2 gene: one in the 3' untranslated region of the gene and one 1200 bp 5' to the gene. It is likely that one or both of these viral insertions is(are) involved in activation of IL-2 expression. We investigated the ability of sequences within the LTR of MLA 144 cells (GALV-MLA) to act as transcriptional elements and have demonstrated here the presence of cis-acting sequences in the GALV LTR capable of enhancing transcription of the GALV promoter as well as two heterologous promoters, SV40 early and IL-2. The results indicate that insertion of the enhancer element(s) alone is not sufficient to activate IL-2 expression but can enhance levels of IL-2 expressed from the activated gene.
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PMID:Transcriptional activity of the gibbon ape leukemia virus in the interleukin 2 gene of MLA 144 cells. 303 78

The interleukin 2 (IL-2) receptor system plays a key role in the T-cell immune response. Although IL-2 binding was reported to be restricted to the Tac peptide, we have identified an IL-2 binding peptide that does not react with anti-human IL-2 receptor monoclonal antibodies, including anti-Tac on MLA 144, a gibbon ape T-cell line. The MLA 144 cell line expressed 6800 IL-2 binding sites per cell with a low (Kd = 14 nM) affinity for human recombinant IL-2. Using cross-linking methodology, we demonstrated that the IL-2 binding peptide on MLA 144 is larger (Mr 75,000) than the Tac peptide, which has a Mr of 55,000. An IL-2 binding peptide of similar size (Mr 75,000) was also identified in addition to the Tac peptide (Mr 54,000-57,000) on Hut 102, a human T-cell lymphotrophic virus I-induced T-cell leukemia line, and phytohemagglutinin-activated normal human and gibbon ape lymphoblasts. Anti-Tac antibody did not block the binding of 125I-labeled IL-2 to MLA 144 cells. However, this antibody abolished the binding of 125I-labeled IL-2 not only to the Tac peptide on Hut 102 cells and normal lymphoblasts but also to the Mr 75,000 IL-2 binding peptide, suggesting that this latter peptide is associated with the Tac peptide to form the high-affinity IL-2 receptor complex.
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PMID:Demonstration of a non-Tac peptide that binds interleukin 2: a potential participant in a multichain interleukin 2 receptor complex. 309 89

Autologous lymphocyte populations from different phases of chronic granulocytic leukaemia (CGL), acute myeloid leukaemia (AML) and preleukaemic disorders were compared for cytotoxic activity. 51Cr-release tests showed that T lymphocytes from the quiescent phase of CGL and from the remission phase of AML exerted cytotoxic activity against autologous tumour cells. Such activity was also found in patients with potentially preleukaemic haematological disorders characterized by cytopenia, but not in polycythaemia vera patients. In the majority of cases cytotoxic activity of T lymphocytes could be blocked by native gp70 antigens of gibbon ape leukaemia virus (GaLV) and baboon endogenous virus (BaEV). Blocking effect of carbohydrate-free gp70 as well as p15(E) antigens could be observed less frequently. The role of cell-mediated immune response to oncovirus antigens in the course of myeloproliferative diseases is discussed.
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PMID:Cytotoxic activity of lymphocyte subpopulations against autologous tumour cells in patients with myeloid leukaemias and preleukaemic disorders. 326 Jul 9

Lymphocyte and plasma samples from the quiescent and blastic phase of chronic granulocytic leukaemia (CGL) and from the blastosis and remission of acute myeloid leukaemia (AML), were compared for cytotoxic activity. Target cells were collected from the blastic phases of diseases. 51Cr-release tests showed that the lymphocytes and plasma samples from blastic crisis of CGL had no cytotoxic activity for autologous blast cells. In contrast, cryopreserved lymphocytes and plasmas from the quiescent phase of CGL proved to be cytotoxic for the autologous tumor cells, and their effect could be blocked by native gp70 antigens of gibbon ape leukaemia virus (GaLV) and baboon endogenous virus (BaEV). A blocking effect was less frequently exerted by carbohydrate-free gp70 and p15(E) antigens. A similar relationship was found between the blastosis and remission stage of AML, however, out of the antigens of BaEV only the native gp70 showed a marked blocking effect.
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PMID:Cytotoxicity of lymphocytes and antibodies against autologous tumor cells in patients with myeloid leukaemias and preleukaemic disorders. III. Stage-dependence of oncovirus-specific immune response. 349 51

The gibbon ape leukemia virus (GALV) contains enhancer activity within its long terminal repeat. In the GALV Seato strain this activity resides in a 48-base-pair (bp) repeated element. We demonstrate the existence of a cellular protein which binds in this region of the Seato strain. A sensitive method for enriching protein-DNA complexes from crude extracts coupled with exonuclease and DNase footprint analysis revealed the specific binding of this protein to a 21-bp region within each repeated element. A 22-bp oligonucleotide fragment defined solely by the 21-bp footprint binds a protein in vitro and displays enhancer activity in vivo, suggesting that this protein is a major determinant of GALV enhancer activity. The protein is present in three cell lines which are positive for enhancer activity and is not detected in Jurkat cells, which are negative for enhancer activity. Only GALV long-terminal-repeat variants which support high levels of enhancer activity in vivo compete with this protein for specific binding in vitro, suggesting a potential role for the protein in determining enhancer activity. This protein binding is not inhibited by competition with heterologous retroviral enhancers, demonstrating that it is not a ubiquitous retroviral enhancer binding protein.
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PMID:Binding of a cellular protein to the gibbon ape leukemia virus enhancer. 367 Feb 91

Normal human cells express a human-specific antigen, HuLy-m5 (defined by the E4.3 monoclonal antibody), cross-reactive with determinants of the primate retroviruses, MPMV(Mason Pfizer monkey virus) and GALV (gibbon ape leukemia virus). Purified virus preparations of MPMV and GALV absorbed E4.3 antibody activity while antisera to these retroviruses blocked the binding of E4.3 antibody to human target cells. Sequential immunoprecipitation and two-dimensional gel analysis both indicated that the anti-primate retrovirus sera recognize the same molecular entity (a two-chain glycoprotein of Mr60 and 69Kd) as does the E4.3 antibody. These results suggest that normal human cells express primate retroviral proteins (most probably viral envelope glycoprotein, gp69) at the cell surface.
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PMID:Cross-reactivity of a normal human cell surface antigen with primate retrovirus glycoproteins. 392 65

A radioimmunoassay for the major, group-specific antigen (p30) of hamster type C viruses was developed. The test detected approximately 5 ng of viral protein per ml and was highly specific for hamster viruses when used with homologous antibody. Comparison of three hamster viruses, two being mouse-hamster pseudotypes, in homologous and heterologous intraspecies assays, showed no evidence of type specificity for these proteins. The pseudotype viruses showed no evidence of mouse virus p30 antigenic determinants. An interspecies antigen assay employing (125)I-labeled hamster p30 and anti-feline p30 was completely inhibited by cat (feline leukemia virus), hamster, and rat viruses, to a slightly lesser degree by mouse viruses, and only poorly by RD 114 and Gibbon ape viruses. The Mason-Pfizer virus did not inhibit this assay. Hamster p30 was detected by radioimmunoassay in individual embryos from two LSH hamsters and in several adult tissues, excluding muscle at levels below that required for detection in complement-fixation tests.
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PMID:Radioimmunoassay for the major structural protein of hamster type C viruses. 413 82

Two strains of feline leukemia virus, two endogenous feline type-C viruses (RD/CCC group), several endogenous and laboratory strains of murine "leukemia" virus, two rat viruses, two primate viruses (woolly monkey and gibbon ape), as well as hamster, pig, and avian type-C viruses were examined for their relatedness to one another by molecular hybridization. The extent of nucleic-acid homology was determined by hybridization of the various viral RNAs to a [(3)H]DNA product synthesized from each virus. Among the murine type-C viruses (Rauscher, Kirsten, AT-124, and endogenous BALB/c virus) a high degree of homology is observed, although the viruses are not identical. The two primate viruses are also closely related to one another. The feline, rat, hamster, and pig endogenous viruses can be readily distinguished from one another and from the murine and primate viruses since their DNA products share very little or no nucleic-acid homology. However, the murine and primate type-C virus groups possess a surprising degree of relatedness. Feline type-C viruses fall into two distinct groups, the feline leukemia virus group and the RD-114/CCC group, with little detectable nucleic-acid homology between them. Infection of feline or rat cells with type-C virus results in production of the endogenous type-C virus of the species along with the infecting virus.
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PMID:Homology between type-C viruses of various species as determined by molecular hybridization. 435 65


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