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Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

(A/J X C3H/HeJ) F1 mice reject somatic cell hybrids of ASL-1 cells (A origin) and LM(TK)- cells (C3H origin), but die from leukemia within 10 days after the inoculation of approximately 10(6) viable ASL-1 cells. Mice rejecting hybrid cells survive for prolonged periods after challenge with otherwise lethal numbers of ASL-1 cells. The hybrid cells, rejected by syngeneic F1 recipients, retained their oncogenic potential as determined by the appearance and progressive growth of tumors in immunologically deficient nu/nu mice injected with the cells. Similar results were obtained using hybrids of a radiation-induced cell line (RADA-1), maintained by serial transfer in strain A mice and LM(TK)- cells. Syngeneic mice injected with RADA-1 X LM(TK)- cells failed to form tumors. Mice rejecting RADA-1 X LM(TK)- hybrid cells survived for prolonged periods after challenge with otherwise lethal numbers of RADA-1 cells.
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PMID:Resistance to murine leukemia in mice rejecting syngeneic somatic hybrid cells. 125 47

A cultured cell line of mouse fibroblasts was transfected with DNA from murine leukemia cells expressing a previously characterized tumor-associated antigen. Antigen-positive cells were used as immunogens in an immunotherapy protocol to determine if they stimulated resistance to the malignant proliferation of the leukemia in susceptible mice. For the experiments, LM(TK-) mouse fibroblasts, a thymidine kinase-deficient mouse cell line, were cotransfected with DNA from ASL-1 murine leukemia cells and the plasmid pSV2neo conferring resistance to Geneticin. Integration of the plasmid into cellular DNA was confirmed by restriction digest blot analysis. A/J mice, highly susceptible to the malignant proliferation of passively transferred ASL-1 leukemia cells, were immunized with the transfected cells. Animals receiving two prior injections of antigen-positive transfected cells and then challenged with an injection of viable ASL-1 cells survived longer than animals in the unprotected control group or in the group receiving immunizations with LM(TK-) cells transfected with plasmid only (p less than 0.01). Some of the mice appeared to have rejected the tumor and lived more than 80 days. One group of protected animals rechallenged with a second injection of ASL-1 cells, 40 days after the first, survived for more than 50 additional days, without evidence of recurrent disease.
Leukemia 1987 Mar
PMID:Immunity to murine leukemia induced in susceptible mice by transfected mouse fibroblasts. 282 15

ASL-1 leukemia X LM(TK-) fibroblast hybrid cells prolong the livers of leukemic (A/JXC3H/HeJ)F1 mice. The hybrid cells, like the fibroblast cells used in forming the hybrid, have lost malignant growth properties in immunocompetent recipients and are rejected. Mice receiving hybrid cells along with ASL-1 cells exhibit immunity toward the leukemia cells; approximately 50% of the animals injected with 10(6) or more hybrid cells along with ASL-1 cells survive more than 60 days; animals in the control group injected with leukemia cells alone invariably die in shorter intervals. The immunity generated is persistent for at least 6 months. Some leukemic mice receiving doses of combination chemotherapy which are insufficient to cure them of the disease survive for prolonged and at times indefinite periods if they are injected with hybrid cells. The immunity generated in mice receiving hybrid cells is directed toward a leukemia-associated antigen of leukemia cells expressed by hybrid cells as well. In mixed lymphocyte culture a heightened stimulation of spleen cells from hybrid cell-injected mice toward ASL-1 cells is observed.
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PMID:Leukemia X fibroblast hybrid cells prolong the lives of leukemic mice. 315 80

Clonogenic assays for M, GM, and G precursors of rat or mouse marrow cells were performed in the presence of medium conditioned by the growth of ASL-1 leukemia X LM fibroblast hybrid cells. Both GM- and M-colony-forming units (CFUs) were present in marrow cultures maintained in conditioned medium (CM) from hybrid cells (up to 162 +/- 10 total colonies per 10(5) cells) and from LM cells (65 +/- 5). Conditioned medium from ASL-1 cells did not lead to the formation of CFUs. The hybrid cell-derived CM supported the development of M and GM-CFUs from the marrows of DBA, CAF1, BDF1, C3D2F1, and C57B1/6 mice as well as Lewis, Brown Norway, and Wistar Furth rats. G-CFU were not detected in any of the preparations. Hybrid cell-CM supported the long-term growth and proliferation of macrophage-like cells from mouse spleen, consistent with the presence of M-colony-stimulating factor (CSF). Evidence that M-CSF formed by the hybrid cells and M-CSF formed by L cells shared structural features was provided by antibody neutralization studies. The CFU-promoting activity of hybrid cell-derived M-CSF was neutralized by an antiserum raised in goats against M-CSF purified from L cells. Independently prepared ASL-1 X LM hybrid cells, like the original, led to the formation of GM and M-CFUs. Attempts to detect each of several other previously defined growth factors in medium conditioned by the hybrid cells were unsuccessful. Interleukins 1, 2, and 3; B cell growth factors interferons alpha, beta, and gamma; erythropoietin; and burst promoting factor were not detected.
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PMID:Formation of macrophage (M) colony-stimulating factor by murine leukemia x fibroblast hybrid cells. 349 13

ASL-1 x LM(TK-) hybrid cells, an established murine leukaemia x fibroblast hybrid cell line, augment the antibody response to sheep red blood cells in inbred mice, as determined by the plaque assay method. The intraperitoneal injection of viable hybrid cells or of growth medium conditioned by the cells leads to an increase both in the total number as well as the proportion of cells forming antibodies to sheep red blood cells. CSF-1, (M-CSF), is detected by radioimmunoassay in the medium conditioned by the hybrid and LM(TK-) cells, but not ASL-1 parental cells. Prior treatment of the conditioned medium with CSF-1 antiserum reduces its capacity to augment the antibody response, and its proliferative stimulus on cells from the marrow indicating that CSF-1 may be at least partly responsible for the adjuvant effect observed. The intraperitoneal implantation of diffusion chambers containing viable CSF-1 producing hybrid cells, like the cells themselves, also leads to an increase in the number of spleen cells forming antibodies to sheep red blood cells.
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PMID:Leukaemia x fibroblast hybrid cells augment the antibody response to sheep red blood cells in inbred mice. 390 92

The antiserum raised in (C3H/HeJ X A/J)F1 mice by repeated immunization with mitomycin c(MMC)-treated ASL-1 leukemia cells maintained in vivo reacted with all tumor and normal cell lines maintained in vitro, but not with cell lines maintained in vivo. The common antigens detected in tissue-culture cells (CATC) turned negative after short in vivo cultivation of in vitro ASL-1 cells, and turned positive after short in vitro cultivation of in vivo ASL-1 cells. Treatment of cultured cells with antibiotics (kanamycin, gentamycin) did not alter the reactivity to the a-CATC serum. However, the activity of a-CATC serum was reduced by mixing the anti serum with fetal bovine serum (FBS), and an antigen antibody precipitation reaction occurred between the serum and FBS. Antigens which reacted with this antiserum were indicated to be FBS-related. The antibody against FBS was incidentally produced by immunization with weakly immunogenic tumor cells treated with MMC in FBS-supplemented medium. This study reinforms that the presence of FBS bound to cell membranes can introduce artifacts in the serological analysis of antiserum.
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PMID:A study on an artifact introduced by fetal bovine serum-supplemented medium. 401 11

The immunogenicity of X-irradiated hybrid cells derived from fusion of ASL-1 leukemia (A origin) and LM (TK-) fibroblasts (C3H origin) was compared to X-irradiated parental ASL-1 leukemia cells maintained in vivo (V-ASL-1) and to X-irradiated ASL-1 leukemia cells maintained in vitro (C-ASL-1). Immunization with hybrid cells induced transplantation resistance against tumor rechallenge with V-ASL-1 more effectively than did immunization with V-ASL-1 tumor cells. Immunization with X-irradiated C-ASL-1 cells produced the same, or slightly stronger level of transplantation resistance than that with X-irradiated hybrid cells. These findings were observed both in A/J and in (C3H/HeJ X A/J)F1 mice. These results raise a question about whether the apparent increased immunogenicity of hybrid cells is due to a result of cell fusion or a result of their growth in vitro.
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PMID:Immunoprotective capability of somatic hybrid cells in comparison with parental tumor cells maintained in vitro. 402 76

The quantity of receptors expressed by specialized cells for hormones, foreign antigenic substances, and other chemical stimuli diminishes after they associate with ligands, correlating with a specific reduction in the responsiveness of the cell to further stimulation. Ligand-induced adaptation of membrane receptors may be akin to antigenic modulation--the reversible disappearance of membrane-associated determinants stimulated by specific antibodies. Antigenic modulation has been studied extensively in the thymus-leukemia (TL) system of mouse leukemias. Antibody-induced changes in the quantities of TL antigens expressed by ASL-1 and RADA-1 cells, independently arising leukemia cell lines of strain A mice, are outgrowths of their metabolic turnover. After interacting with TL antibodies, the rate of TL antigen disappearance from the membrane increases while the rate of antigen synthesis remains unchanged. Antiserum with specificities for two membrane-associated determinants of ASL-1 cells, TL and a tumor-associated antigen, leads to modulation of TL antigens alone; the tumor antigen persists. Selectivity of modulation is taken as an indication that complex cellular controls govern the affect of antiserum on the expression of membrane antigens. To detect the presence of regulatory controls governing the expression of membrane determinants, stable somatic hybrids of ASL-1 murine leukemia cells and LM(TK)- cells, a sustained mouse cell line, were prepared and antiserum affects on membrane antigen expression were investigated. The metabolic half-lives of each of three antigen determinants investigated was distinct from the others examined. The hybrid cells have lost their capacity to mudulate TL antigens. TL antigens of hybrid cells, unlike those of parental ASL-1 cells, continue to be expressed in the presence of high titers of TL antiserum. Similarities between antigenic modulation and down regulation exist, among which are the fate of receptor-ligand complexes, changes in their metabolism after binding to ligand, and the dependence of the reactions upon continued sources of cellular energy.
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PMID:Adaptation of membrane-associated determinants is an outgrowth of their metabolism. 624 90

We have investigated the number of structural genes present in ASL-1 cells, a murine leukemia cell line which encodes the heavy chain of thymus leukemia (TL) antigens, a protein which is similar to the Class I histocompatibility antigens. TL-specific messenger RNA was purified from polysomes of ASL-1 cells by immunoprecipitation, and this messenger RNA translated in vitro to produce a Mr 42,000 protein which comigrated on acrylamide gel with nonglycosylated TL heavy chain. A 32P-labeled complementary DNA (cDNA) was synthesized by reverse transcription of the TL-specific messenger RNA as template. Analysis of reassociation kinetics of the 32P-TL-cDNA with DNA from ASL-1 cells showed that the kinetics was indistinguishable from that obtained using a DNA encoding a single-copy gene (C mu). An analysis was performed in which DNA from ASL-1 cells was subjected to digestion with each of three restriction enzymes and hybridized with 32P-TL-cDNA according to the Southern "blot" technique. Two bands formed hybrids with the 32P-TL-cDNA with each of three restriction enzymes used. These data are consistent with the presence of a small number of structural genes for the TL heavy chain in the genome of ASL-1 leukemia cells.
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PMID:Estimation of the number of genes specifying the heavy chain of mouse thymus leukemia antigens. 630 82

Somatic hybrids of ASL-1 leukaemia cells and LM(TK-) fibroblast cells, established mouse cell lines, are rejected by immunocompetent histocompatible mice; however, they grow progressively in nude mice and proliferate indefinitely in vitro. Mice rejecting such hybrid cells exhibit immunity toward ASL-1 leukaemia cells, used as one of the parents in forming the hybrid. In histocompatible recipients, ASL-1 cells are highly malignant, but LM(TK-) cells are rejected. Several distinguishing characteristics in the properties of the surface antigens of the three cell types are described. ASL-1 cells and hybrid cells but not LM(TK-) cells form an antigenically cross-reactive leukaemia-associated antigen; however, it is not detected on the surface membranes of ASL-1 cells taken directly from leukaemic mice. The antigen becomes apparent after short-term culture of the cells. Serum from leukaemic animals, unlike specific antibodies, has no effect upon the expression of the leukaemia-associated antigen of either hybrid or ASL-1 cells. Hybrid cells form a 'second' antigen, foreign to F1 mice, which can be distinguished from the leukaemia-associated antigen of ASL-1 cells. It is not detected on either parental cell. The leukaemia-associated antigen of ASL-1 cells is more readily digested by each of three proteases used than the analogous antigen of hybrid cells. The heightened immunogenic properties of hybrid cells is reflected by the observation that spleen cells from mice injected with hybrid cells undergo extensive proliferation in short-term in vitro culture, with or without an added specific stimulus.
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PMID:Surface antigens of immunoprotective leukaemia x fibroblast hybrid cells which have lost malignant properties in histocompatible mice differ from the malignant parental cells. 637 36


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