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)

Adult BALB/c mice were injected with Moloney sarcoma virus (MSV) after which the animals' lymphocytes were examined for activity against Moloney leukemia virus (MLV) antigen-bearing target cells at 5-day intervals for 30 days. Lymphocytes from these animals and appropriately matched controls were fractionated into B cell-deficient (primarily T cells) and T cell-deficient (primarily B cells) subpopulations. Macrophages were removed using iron powder and magnetism. The unfractionated lymphocytes, T cells, and non-T cells were then tested in microcytotoxicity tests. Antigen-specific activity was found in the unfractionated lymphocytes from animals that had not yet developed palpable tumors and from regressor animals. The T cells were active just before tumor development and just after regression; however, by day 30 after virus infection (8-10 days after regression) the T cell subpopulation was much less active. The non-T cell subpopulation was also active before tumor development and soon after regression. However, this activity continued to rise after regression and was highest at 30 days. At day 15 (peak tumor size) neither subpopulation was active. The activity was demonstrated to be specific for the MLV-determined cell surface antigen by testing on control target cells that were MLV antigen negative and by comparison of the inhibitory effects with lymphocytes immune to a nonpertinent antigen as well as normal lymphocytes. The non-T cells were tested for activity before and after removal of macrophages with iron powder and magnetism. Such cells were significantly more active after removal of the macrophages. These data demonstrate specific T cell and non-T cell activity in microcytotoxicity tests with a tumor-specific system and strongly suggest that the non-T cell activity described herein is a B cell function.
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PMID:The lymphocyte response to primary Moloney sarcoma virus tumors in BALB-c mice. Definition of the active subpopulations at different times after infection. 470 69

This report concerns a cell surface antigen (G(IX); G = Gross) which exhibits mendelian inheritance but which also appears de novo in cells that become productively infected with MuLV (Gross), the wild-type leukemia virus of the mouse. In normal mice, G(IX) is a cell surface allo-antigen confined to lymphoid cells and found in highest amount on thymocytes. Four categories of inbred mouse strains can be distinguished according to how much G(IX) antigen is expressed on their thymocytes. G(IX) (-) strains have none; in the three G(IX) (+) categories, G(IX) (3), G(IX) (2), and G(IX) (1), the amounts of G(IX) antigen present (per thymocyte) are approximately in the ratios 3:2:1. A study of segregating populations derived mainly from strain 129 (the prototype G(IX) (3) strain) and C57BL/6 (the prototype G(IX) (-) strain) revealed that two unlinked chromosomal genes are required for expression of G(IX) on normal lymphoid cells. The phenotype G(IX) (+) is expressed only when both genes are present, as in 129 mice. C57BL/6 carries neither of them. At one locus, expression of G(IX) is fully dominant over nonexpression (G(IX) fully expressed in heterozygotes). At the second locus, which is linked with H-2 (at a distance of 36.4 +/- 2.7 units) in group IX (locus symbol G(IX)), expression is semidominant (50% expression of G(IX) in heterozygotes); gene order T:H-2:Tla:G(IX). As a rule, when cells of G(IX) (-) mice or rats become overtly infected with MuLV (Gross), an event which occurs spontaneously in older mice of certain strains and which also commonly accompanies malignant transformation, their phenotype is converted to G(IX) (+). This invites comparison with the emergence of TL(+) leukemia cells in TL(-) mouse strains which has been observed in previous studies and which implies that TL(-) --> TL(+) conversion has accompanied leukemic transformation of such cells. So far the only example of G(IX) (-) --> G(IX) (+) conversion taking place without overt MuLV infection is represented by the occurrence of GCSA(-):G(IX) (+) myelomas in BALB/c (GCSA:G(IX) (-)) mice. Unlike the other Gross cell surface antigen described earlier, GCSA, which is invariably associated with MuLV (Gross) infection and never occurs in its absence, G(IX) antigen sometimes occurs independently of productive MuLV infection; for example, thymocytes and some leukemias of 129 mice are GCSA(-):G(IX) (+), and MuLV-producing sarcomas may be GCSA(+):G(IX) (-). The frequent emergence of cells of G(IX) (+) phenotype in all mouse strains implies that the structural gene coding for G(IX) antigen is common to all mice. There is precedent for this in the TL system, in which two of the Tla genes in linkage group IX appear to be ubiquitous among mice, but are normally expressed only in strains of mice carrying a second (expression) gene. It is not yet certain whether either of the two segregating genes belongs to the MuLV genome rather than to the cellular genome. This leaves the question whether MuLV may have a chromosomal integration site still debatable. But there is a good prospect that further genetic analysis will provide the answer and so elucidate the special relationship of leukemia viruses to the cells of their natural hosts.
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PMID:The G-IX system. A cell surface allo-antigen associated with murine leukemia virus; implications regarding chromosomal integration of the viral genome. 557 34

Before 1980, infectiously transmitted human retroviruses were unknown. Since then three types of human T-lymphotropic viruses (HTLVs) have been discovered and are under intensive study. Further types may well come to light. HTLV-I is etiologically associated with adult T-cell leukemia-lymphoma (ATLL), HTLV-II has been isolated from a patient with hairy T-cell leukemia, and HTLV-III is the cause of acquired immune deficiency syndrome (AIDS). Viruses related to HTLVs occur in several species of macaque monkeys. It appears that only a small minority of infected subjects develop the associated malignancy or immunodeficiency. Little is known of HTLV transmission, although it is clear that the viruses can be transmitted sexually and also iatrogenically through blood. HTLV-I and HTLV-II appear to be highly conserved across different human host populations, whereas HTLV-III shows greater polymorphism and elicits different immune responses. HTLVs have a tropism for T-helper/inducer cells. While HTLV-I and HTLV-II can penetrate many cell types and the T-cell tropism may reside in the activity of the X gene product following infection, initial infection of HTLV-III is restricted to cells bearing the T4 cell surface antigen. The T4 antigen is an essential component of the receptor for the virus, which is consistent with its tropism and the nature of the immunodeficiency it causes.
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PMID:Human retroviruses in health and disease. 610 Jun 47

Genes in the D region of the murine major histocompatibility complex, H-2, confer resistance to radiation-induced leukaemia virus. H-2D gene control appears to ensue at a step subsequent to virus infection, since elimination of virus infected cells does not become apparent until 3--5 weeks after virus infection. Nonetheless, almost immediately after virus infection, expression of H-2D-coded antigens is markedly elevated on the surface of thymocytes from resistant (H-2Dd) but not susceptible mice (H-2Ds or H-2Dq). This increased H-2D antigen expression triggers a vigorous cell-mediated immune response which probably plays a key role in resistance to leukaemia via elimination of virus-infected cells. A hypothesis is put forth to explain the induction of increased sythesis and expression of H-2D antigens. This hypothesis postulates that the oncogenic segment of RadLV bears a close resemblance to H-2.4, the private specificity for H-2Dd, allowing it to integrate at or near the H-2Dd murine gene. Subsequent to integration, the rates of transcription and translation are altered with a resulting increase in cell surface antigen expression. Other possibilities are also discussed.
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PMID:H-2D control of leukaemia susceptibility: mechanism and implications. 615 52

Antibody-secreting hybridomas were produced by fusion of P3-NS1/1Ag--4-1 mouse plasmacytoma cells with splenocytes from a mouse immunized with HL-60 human promyelocytic leukemia cells. A cloned hybridoma cell line was identified that secreted antibody against a cell surface antigen expressed on all normal human peripheral blood granulocytes, on bone marrow granulocytic precursor cells, and on blast cells from 3 of 15 patients with nonlymphoid leukemia. However, the antibody did not react with normal peripheral blood lymphocytes, monocytes, platelets, or red cells, or with blast cells from 20 patients with acute lymphoblastic leukemia or from 5 patients with lymphoma. This monoclonal antibody identified a granulopoietic differentiation antigen (designated My-1) and may prove useful in the subclassification on nonlymphoid leukemia and in the investigation of hematopoiesis.
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PMID:My-1, new myeloid-specific antigen identified by a mouse monoclonal antibody. 616 93

The AKR.H-2bSL1 tumor cell line is susceptible to H-2Kb-restricted cytotoxic T lymphocytes (CTL) directed against the subclass of AKR endogenous leukemia virus-induced tumors that express the Gross cell surface antigen (anti-AKR/Gross virus CTL). A variant subclone (cl.18-5) of AKR.H-2bSL1 was isolated, whose susceptibility to lysis by conventional or cloned lines of anti-AKR/Gross virus CTL was approximately 5% or less than that of the parental tumor. The cl.18-5 variant was also ineffective when used as an in vivo priming cell or an in vitro stimulator cell in the generation of anti-AKR/Gross virus CTL or as an unlabeled target cell in competitive inhibition assays. These results implied that the failure of cl.18-5 to be lysed was due to a lack of recognition by the CTL. In contrast, cl.18-5 was able to be lysed by and stimulate the generation of predominantly H-2Db-restricted CTL with apparent specificity for AKR minor histocompatibility antigens. The variant line was also about as susceptible as the parental AKR.H-2bSL1 line to both allogeneic CTL and to H-2Kb-restricted, TNP-specific CTL. Thus, the lack of recognition of cl.18-5 by anti-AKR/Gross virus CTL did not appear to be due to a failure to express functional H-2 products or to a generalized insusceptibility to H-2-restricted CTL. Rather, cl.18-5 appeared to be a selective variant and a useful probe for studying the specificity of anti-AKR/Gross virus CTL.
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PMID:The specificity of H-2-restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus-induced tumors. I. Isolation of a selectively resistant variant tumor subclone. 619 6

Derived from the susceptible AKR.H-2bSL1 tumor cell line, a variant tumor subclone, cl.18-5, was selectively insusceptible to H-2-restricted anti-AKR/Gross virus cytotoxic T lymphocytes (CTL) due to its failure to be recognized. In this study, the expression of virus-related products by variant cl.18-5 cells was compared to that of AKR.H-2bSL1 cells and a susceptible clone, as an approach towards defining the virus-associated antigens recognized by anti-AKR/Gross virus CTL. Despite the type specificity of the CTL, cl.18-5 displayed normal levels of the group-specific antigen (gag) encoded proteins p30, p15, p12 and p10, and the gag-associated Gross cell surface antigen. These results were confirmed by fluorescence-activated cell sorter analysis employing monoclonal antibodies specific for either AKR p12 or the cell surface glycosylated form of AKR ecotropic gag product. In contrast, cl.18-5 was variably less sensitive than AKR.H-2bSL1 to the action of complement and xenogeneic antisera directed against the envelope (env) product gp70. In addition, a panel of five monoclonal antibodies to gp70, which detect distinct endogenous ecotropic viral determinants, lysed AKR.H-2bSL1, but not cl.18-5 cells. However, absorption experiments indicated that cl.18-5 did express near normal levels of these specificities, suggesting an alteration in the orientation or topographical distribution of these determinants. Consistent with an inappropriate display of env products, cl.18-5 was found to be deficient in the production of infectious ecotropic leukemia virus. The particulate fraction of the cell-free supernatant of cl.18-5 contained normal levels of reverse transcriptase activity, indicating that noninfectious viral particles were being produced. Collectively, these results point to an association between recognition by anti-AKR/Gross virus CTL and the expression of ecotropic gp70 required for infectivity of virus.
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PMID:The specificity of H-2-restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus-induced tumors. II. Altered gp70 display and production of noninfectious virus particles by an insusceptible variant tumor. 619 7

Murine leukemia viruses isolated from radiation-induced BALB/c leukemias were characterized with respect to viral proteins and RNA. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the viral structural proteins revealed that for p12, p15, p30, and gp70, three of four electrophoretic variants of each could be detected. There was no correlation found between any of these mobilities and N- or B-tropism of the viruses. Proteins of all xenotropic viral isolates were identical in their gel electrophoretic profiles. The similar phenotypes of multiple viral clones from individual leukemias and of isolates grown in different cells suggest that the polymorphism of ecotropic viruses was generated in vivo rather than during in vitro virus growth. By two-dimensional fingerprinting of RNase T1-resistant oligonucleotides from 70S viral DNA, the previously reported association of N- and B-tropism with two distinct oligonucleotides was confirmed. The presence of two other oligonucleotides was correlated with positive and negative phenotypes of the virus-coded GIX cell surface antigen. The RNAs of two B-tropic isolates with distinctive p15 and p12 phenotypes differed from the RNA of a prototype N-tropic virus by the absence of three oligonucleotides mapping in the 5' portion (gag region) of the prototype RNA. In addition, one small-plaque B-tropic virus displayed extensive changes in the RNA sequences associated with the env region of the prototype.
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PMID:Biochemical analysis of murine leukemia viruses isolated from radiation-induced leukemias of strain BALB/c. 625 Dec 40

Functional studies of lymphocyte subpopulations reveal that Ly 11.2, a newly defined T cell surface antigen, is present on prothymocytes and natural killer cells, but not on suppressor T cells for antigen-specific IgE antibody responses, Ly 1+, 2-, 3- helper T cells nor on tumor-specific cytotoxic effector cells. Changes in the expression of Ly 11.2 regularly accompany leukemogenesis and are quite distinct from changes of other cell surface antigens thus far observed. After intrathymic inoculation of radiation leukemia virus (RadLV), many more Ly 11.2-positive cells are found expressing viral antigens than cells expressing other cell surface phenotypes. In addition, after RadLV inoculation, significantly more Ly 11.2-positive cells can be found in the thymus of susceptible mice than in the thymus of resistant mice. The greater availability of permissive (Ly 11.2-positive) cells in susceptible vs resistant hosts at the time when infectious virus is present may account for the shorter latency period and high leukemia incidence of susceptible vs resistant mice.
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PMID:Functional properties of Ly 11.2 lymphocytes: a role for these cells in leukemia? 625 69

A new cell surface antigen of the mouse related to xenotropic murine leukemia virus (MuLV) is described. The antigen, designated G(erld), is defined by cytotoxic tests with the B6-x-ray-induced ERLD and naturally occurring antibody. G(erld) is distinct from all previously defined cell surface antigens. Monoclonal antibody with the same specificity has been developed. Inbred mouse strains are classified as G(erld)+ or G(erld)- according to the presence of absence of the antigen on lymphoid cells. G(erld)+ strains differ with regard to quantitative expression of G(erld) on normal thymocytes. The emergence of G(erld)+ tumors in G(erld)- strains indicates the presence of genes coding for the antigen even in strains not normally expressing the antigen. G(erld) has the characteristic of a differentiation antigen in normal mice. In G(erld)+ strains, high levels of the antigen are found on thymocytes with lower levels being detected on cells of spleen, lymph nodes and bone marrow. No G(erld) was detected in brain or kidney or on erythrocytes. The segregation ratios for G(erld) expression on thymocytes in backcross and F2 mice of crosses between G(erld)+ (B6, 129, and B6-Gix+) and G(erld)- (BALB/c) strains suggest that G(erld) expression is controlled by a single locus in B6, by two unlinked loci in 129, and by three unlinked loci in B6-Gix+ mice. Induction of the antigen by MuLV infection of permissive cells in vitro indicates that G(erld) is closely related to xenotropic and dualtropic MuLV; all xenotropic and dualtropic MuLV tested induced the antigen, whereas the majority of ecotropic and the two amphotropic MuLV failed to do so. As dualtropic MuLV are thought to be recombinants between ecotropic and xenotropic MuLV sequences, G(erld) coding by dualtropic MuLV may signify the contribution of the xenotropic part in the recombinational event. Serological and biochemical characterization indicates that G(erld) is related to the gp 70 component of the MuLV envelope. The relation of G(erld) to the previously defined gp 70-related cell surface antigens (Gix, G(rada), and G(aksl2) is discussed, particularly with regard to their characteristics as differentiation antigens, the genetic origin of dualtropic MuLV, and the leukemogenicity of MuLV.
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PMID:A cell surface antigen of the mouse related to xenotropic MuLv defined by naturally occurring antibody and monoclonal antibody. Relation to Gix G(rada1), G(aksl2) systems of MuLV-related antigens. 626 31


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