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)

RADA-1 cells [H-2a thy-1b; thymus-leukemia (TL) 1, 2, 3], a radiation-induced murine leukemia cell line maintained by serial transfer in histocompatible recipients, resisted lysis by guinea pig complement (GPC) and TL 1, 3; TL 2; or TL 1, 2, 3 antiserum. The cells expressed TL antigenic specificities as determined by indirect fluorescent antibody methods, the direct isolation of TL antigens from the cells, and the capacity of the cells to reduce known titers of TL antisera. GPC was consumed to the same extent during the reaction of resistant cells and TL antisera as occurred in the reaction of sensitive cells (killed under similar conditions) and TL antisera. RADA-1 cells were not nonspecifically resistant to complement (C)-mediated lysis; they were killed in the presence of H-2a antiserum and GPC. The TL antisera contained antibodies for TL determinants. They stimulated the C-mediated lysis of ASL-1 cells (TL 1, 2, 3) and thymocytes from strain A mice (TL 1, 2, 3). The TL antigens of resistant RADA-1 cells underwent antigenic modulation, the reversible disappearance of TL antigens from the cells stimulated by specific antiserum. After the cells were treated with neuraminidase, they became susceptible to the cytotoxic effects of aliquots of the same TL antisera and GPC used previously.
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PMID:Detection of a TL(+) murine leukemia cell line that resists the cytotoxic effects of guinea pig complement and specific antiserum. 5 Oct 85

RADA-1 cells (H-2a), a murine leukemia cell line maintained by serial transfer in histocompatible recipients expressing thymus-leukemia (TL) 1, 2, 3 antigenic determinants, resisted the cytotoxic effects of guinea pig complement (GPC) and TL antiserum. The cells expressed a lower density of TL antigens than did ASL-1 cells, another TL(+) leukemia cell line expressing the same determinants and susceptible to complement (C)-mediated lysis. Stable somatic cell hybrids of RADA-1 cells and LM(TK)- cells (H2k), a TL(minus) thymidine kinase-deficient mutant of mouse L cells, were selected in hypoxanthine-aminopterin-thymidine medium. The hybrid cells expressed the H-2 antigens of both parents and shared a hybrid karyotype. They formed TL 1, 2, 3 antigens as determined by immunofluorescence, mixed hemagglutination methods, the direct isolation of TL antigens from Nonidet P40 extracts of the cells, and the capacity of the cells to reduce by absorption the known titers of TL antiserum. These hybrid cells lost the capacity to resist lysis by TL antiserum and GPC. They were susceptible to the cytotoxic effects of TL 1, 2, 3; TL 2; OR TL 1, 3 antiserum and GPC, even though the density of TL antigens associated with the cells was approximately 25% of their resistant RADA-1 parental cells. These results indicated that the mechanism of resistance to C-mediated lysis was genetically separable from the expression of TL antigens by the cells and that the susceptibility of the cells to the cytotoxic effects of antiserum was related only in part to the density of TL antigens expressed by the cells.
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PMID:Complement sensitivity of somatic hybrids of a complement-resistant murine leukemia cell line. 5 Oct 86

A somatic hybrid of ASL-1 leukemia cells [H-2a, thymus leukemia (TL)1,2,3, Thy-1b] and LM(TK)-cells [H-2-k, TL(-), Thy-1 (-), thymidine kinase deficient] was formed with the aid of inactivated Sendai virus. The selection of hybrid cell clones was facilitated by the inability of ASL-1 cells to grow in vitro and of LM(TK)-cells to survive in hypoxanthine/amethopterin/thymidine medium. The H-2 antigens of both parental cells were formed in approximately equivalent amounts by the hybrid cells, and they possessed a hybrid karyotype. As determined by five independent experimental procedures (antibody and complement-mediated cytotoxicity tests, the reduction of specific antibody activity of antiserum of known titer, immunofluorescent tests, mixed hemagglutination tests, and their direct isolation), TL antigens but not Thy-1 antigens were formed by the hybrid cells. TL antigens of the hybrids failed to undergo modulation under conditions leading to the modulation of TL antigens of parental ASL-1 cells. Modulation was attempted with TL 1,3, TL 2, or TL 1,2,3 antisera of high titer. thybrid cells were incubated for up to 30 hr in medium with TL antisera. Both direct and indirect immune methods were attempted. These results indicate that cellular mechanisms controlling the expression of TL antigens may be distinguished from the capacity of the cells to undergo modulation.
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PMID:Somatic hybrid of thymus leukemia (. 16 80

The expression of the thymus leukemia antigen (TL) was studied on a murine leukemia cell line (ASL-1W) grown in vitro and separated into cell cycle phases by velocity sedimentation or growing synchronously in culture. The expression of TL was determined qualitatively by direct cytotoxicity and quantitatively by a modified inhibition of cytotoxicity assay. TL expression was found to vary with DNA synthesis. The hypothesis that expression is coordinately regulated with DNA synthesis, and the relationship of this to the restricted expression of TL on rapidly dividing cells is disucssed.
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PMID:Selective cell surface expression of thymus leukemia antigen during S phase of the cell cycle. 31 16

The thymus leukemia (TL) antigens of ASL-1 murine leukemia reversibly disappeared from the membranes of cells exposed to TL antisera; the cells acquired resistance to fresh TL antiserum and complement (antigenic modulation). Three independent methods, however, indicated that the acquisition of complement resistance preceded the complete disappearance of TL antigens from the cell surface. Modulated cells reduced known titers of TL antisera by absorption; they stained positively in immunofluorescence studies involving TL antibodies and fluorescence-labeled rabbit anti-mouse immunoglobulin. TL antigens labeled previously with 125I were recovered by immunoprecipitation from cellular extracts prepared with nonionic detergent. Continued exposure of the cells to TL antiserum led to virtually complete disappearance of the antigens. Similar results were obtained for RADA-1 cells, another murine leukemia that forms TL antigens, although in this instance the cells were resistant to the cytolytic effects of TL antisera and guinea pig complement (GPC) without prior exposure to TL antibodies. The density of TL antigens remaining on the surface of different TL(+) cell types failed to correlate with resistance to TL antibodies and GPC. Cells from F, hybrids of TL(+) and TL(-) mouse strains formed TL antigens and were susceptible to TL antibodies and GPC even though the density of TL antigens formed by the susceptible cells was less than the density of TL antigens formed by modulated cells. Stable somatic hybrids of RADA-1 cells and TL(-) cells formed TL antigens at lower density than did RADA-1 cells and lysed in the presence of aliquots of the TL antisera and GPC used in previous tests.
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PMID:Detection of thymus leukemia antigens on the surface membranes of murine leukemia cells resistant to thymus leukemia antibodies and guinea pig complement. 32 93

Previous studies have shown that the cell surface expression of thymus leukemia antigen (TL) on ASL-1w leukemia cells varies with the progression of the cells through the growth cycle. Expression of TL is maximal in S phase, and its quantitative expression varies directly with DNA synthesis. In the present study, the effect of anti-TL serum on the growth of ASL-1w cells was examined. The antiserum, tested in the absence of complement, affected the growth of these cells in biphasic manner. When the antiserum concentration was 0.1% or greater, there was a rapid decline in the rate of DNA synthesis, and after 5 to 7 hr, cell death. When the antiserum concentration was 0.067% or less, the decline in the rate of synthesis of DNA did not become apparent until 5 to 6 hr after treatment. Under these conditions, there was approximately a 20% increase in cell number after 24 hr of culture. The hypothesis that treatment of ASL-1w cells with the lesser concentration of anti-TL serum blocks the cells in G2 phase of the cell cycle is discussed.
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PMID:Inhibition of growth of ASL-1w murine leukemia cells by anti-thymus leukemia antigen (TL) serum in the absence of complement. 48 68

The quantity of thymus-leukemia (TL) antigens expressed by murine leukemia cells is significantly greater than that expressed by somatic hybrids of such cells. Based upon the results of 125I-lactoperoxidase labeling and antibody absorption procedures, and corrected for size differences between the two cell types, the quantity of TL antigens expressed by RADA-1 cells, a radiation-induced murine leukemia cell line of strain A/J mice, is approximately 5.0 times greater than that of somatic hybrids of RADA-1 and LM(TK)- cells. LM(TK)- cells are a thymidine kinase-deficient TL(-) mouse fibroblast cell line. The quantity of TL antigens expressed is related only in part to their susceptibility to lysis by TL antibodies and guinea pig complement (GPC). RADA-1 cells resist lysis. The quantity of TL antigens expressed by RADA-1 cells is analogous to that formed by nonneoplastic thymocytes obtained from F1 hybrids of two strains of TL(+) and TL(-) mice; cells from both strains are sensitive to TL antiserum and GPC. ASL-1 cells, a spontaneously occurring leukemia cell line of A/J mice, express TL antigens in significantly higher quantities than any of the cell types examined. Exposed to TL antisera, the quantity of TL antigens of ASL-1 cells, but not that of hybrid cells, gradually diminishes. ASL-1 cells convert over a 6-h period of exposure to antibody and guinea pig complement (GPC) resistance; hybrid cells remain sensitive. However, ASL-1 cells converted to TL antibody and GPC resistance continue for a time to express TL antigens in quantities similar to that of sensitive F1 thymocytes and resistant RADA-1 cells. RADA-1 X LM(TK)- hybrid cells, which are sensitive to TL antibodies and GPC, express the lowest quantities of TL antigens of any of the cell types examined. It is likely that differences in the quantities of TL antigens expressed by different cell lines reflect genetic mechanisms controlling TL antigen expression. The failure of TL antisera to affect the quantities of TL antigens expressed by hybrid cells is taken as an indication that genetic controls governing antigen expression may be distinguished from those involved in regulating responsiveness to specific antiserum.
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PMID:Murine leukemia cell hybrids: the quantity of TL antigens expressed by parental and hybrid cells fails to correlate with their sensitivity to TL antibody and complement. 75 Jul 64

(A/J x C3H/HeJ)F1 mice (H-2a/k) exhibit no apparent resistance to the malignant proliferation of ASL-1 leukemia cells (H-2a), a spontaneously occurring neoplasm of A/J mouse origin. The period of survival after injections of ASL-1 cells is related to the number of cells introduced into the susceptible host. (A/J x C3H/HeJ)F1 mice receiving viable ASL-1 cells along with ASL-1 x LM(TK)- somatic hybrid cells (H-2a/k), syngeneic with the recipients, survived for statistically significant (p less than 0.001), longer periods than did mice receiving ASL-1 cells alone. Mice receiving ASL-1 and ASL-1 x LM(TK)- hybrid cells together survived for approximately twice as long as animals receiving ASL-1 cells alone. Mice receiving ASL-1 cells followed by hybrid cells survived for longer periods as well, but the therapeutic effects were less successful. ASL-1 x LM(TK)- hybrid cells are rejected after forming localized tumors by the immunocompetent F1 mice. In some instances, F1 animals previously rejecting hybrid cells and challenged subsequently with ASL-1 cells along with a second injection of hybrid cells survived indefinitely. The passive transfer of partial immunity to the leukemic cells could be achieved by injections of spleen cells from F1 mice that had rejected hybrid cells previously. Similar results were obtained for (A/J x C3H/HeJ)F1 mice receiving RADA-1 cells (H-2a), a radiation-induced leukemic line of A/J origin, along with RADA-1 x LM(TK)- hybrid cells (H-2a/k). The partial immunity induced by these lines of hybrid cells was cross-reactive: mice injected with ASL-1 cells and RADA-1 x LM(TK)- hybrid cells survived for prolonged periods, and vice versa.
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PMID:Resistance to murine leukemia in mice receiving simultaneous injections of syngeneic hybrid and parental neoplastic cells. 84 40

Fusion of ASL-1 cells, a murine leukemia forming thymus leukemia (TL) antigens, with LM(TK)- cells, a TL(--) murine cell line, resulted in a stable hybrid forming TL antigens. The hybrids failed to undergo modulation, the reversible dissappearance of TL antigens from the surfaces of the cells, stimulated by TL antiserum. Unlike ASL-1 cells, the rate of disappearance of the antigens from modulation negative hydrid cells was unaffected by TL antiserum. The t 1/2 of TL antigens of the hybrid was approximately 30 h. The t 1/2 of TL antigens of ASL-1 cells was 10 h in the presence of TL antiserum, 18 h in the absence of TL antiserum. The rate of metabolism of a putative tumor-associated antigen of ASL-1 cells formed by the hybrid was unaffected by exposure to specific antiserum, as was the metabolism of H-2 antigens formed by the cell types.
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PMID:The effect of specific antiserum on the metabolism of three membrane-associated antigens of ASL-1 x LM(TK)- hybrid cells. 102 45

The effect of specific antisera on the metabolic rates of thymus-leukemia (TL), H-2a, and tumor-associated antigens of ASL-1 and RADA-1 cells, two murine leukemia cell lines, were determined. The metabolic half-life of each antigen was distinct from the others examined. The half-life of TL antigens was 18 hr; in cells exposed to TL antiserum, it changed to 9 hr. In RADA-1 cells, the half-life of TL antigens was 16 hr; in the presence of TL antiserum it became 4 hr. The half-lives of H-2a antigens and the tumor-associated antigen were unaffected by specific antiserum. Somatic hybrids of ASL-1 or RADA-1 cells were formed with LM(TK)-cells, a thymidine kinase deficient mutant of mouse L cells. Hybrid cells formed TL antigens, but unlike their parental cells their half-life of expression, approximately 30 hr, was unaffected by TL antiserum. Hybrid cells failed to undergo antigenic modulation under conditions more stringent than required to stimulate the modulation of ASL-1 or RADA-1 cells. The hybrids formed the tumor-associated antigen of their murine leukemia parental cells; however, the metabolic rate of the tumor antigen in hybrid cells was defferent than the metabolic rate of the analogous antigen in parental cells. Hybrid cells formed H-2 antigens of both parental sources, and possessed a hybrid karyotype. The half-life of H-2 antigens, approximately 26 hr, was the same both in parental and hybrid cells. H-2a antiserum had no detectable effect upon the metabolism of TL antigens in hybrid or parental cells; nor did TL antiserum have an effect upon the metabolism of H-2a antigens.
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PMID:Independent control of the expression of several membrane-associated antigens of murine leukemia cells: metabolism and response to specific antiserum. 103 Aug 6


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