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)

Antiserum was generated in rabbits to the RPMI 8226 tissue culture line of human myeloma cells, and its reactions with fixed smears of bone marrow aspirates from patients with multiple myeloma, macroglobulinemia, benign monoclonal gammopathy (BMG), leukemia, and nonneoplastic plasmacyosis was assessed by indirect immunofluorescence. After absorption with preparations of bone marrow from normal individuals, the antiserum reacted to a significantly higher titer with a specific subpopulation of plasma cells in smears from 81% of patients having multiple myeloma and 50% of patients having BMG than with cells in smears of bone marrow aspirates from normal individuals or patients having leukemia or nonneoplastic plasmacytosis, or than with cells in smears of peripheral blood from patients having Hodgkin's and non-Hodgkin's lymphoma. Absorption of the antiserum with RPMI 8226 cells or with a bone marrow preparation from a patient with multiple myeloma but not the Jijoye line of Burkitt's lymphoma reduced reactivity for cells in myeloma bone marrow. The antiserum reacted at a lower titer with the Jijoye and EB-3 lines of Burkitt's lymphoma, the RPMI 4098 cell line of normal human lymphocytes, and culture lines of human melanoma and osteogenic sarcoma than with the RPMI 8226 cells or bone marrow from certain patients having multiple myeloma. Approximately 50% of the cells reactive with antiserum to RPMI 8226 cells in the bone marrow of patients with multiple myeloma were not producing immunoglobulin, as assessed by double immunofluorescence assay. The data suggested that a subpopulation of plasma cells in the bone marrow of patients with multiple myeloma possesses a tumor-associated antigen.
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PMID:Tumor-associated antigens in human myeloma. 5 51

The antigenicity of tumor-associated antigen (TAA) was compared between 3-methylcholanthrene-induced rat fibrosarcoma KMT-17 and Friend murine leukemia virus-infected KMT-17 (FV-KMT-17) cells. The antigenicity was classified into immunosensitivity and immunogenicity, and studied from the viewpoint of humoral immunity. The immunosensitivity to anti TAA antibodies increased by artificial infection of KMT-17 cells with Friend virus. The results suggested that an increase of lateral mobility of TAA on the cell surface contributes to the increase of immunosensitivity. Concerning the immunogenicity of TAA, an augmentation of anti-TAA antibody formation was demonstrated when FV-KMT-17 cells were used as the immunogen. In this case, a physical association between TAA and virus-associated antigen (VAA) was suggested to be very important to increase the immunogenicity of TAA.
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PMID:Topographical distribution and association of tumor--associated antigens and their role in antigenicity in rat tumor cells. 9 61

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

Cell-mediated immunity (CMI) and tumor rejection were studied in the Friend virus leukemia system of C57Bl/6 mice. Mice were immunized with Friend leukemia virus (FLV) or X-irradiated FBL-3 leukemic cells and studied temporally for the development of CMI reactivity by assays of 51Cr release lymphocyte cytotoxicity, lymphocyte transformation, migration inhibition, Winn tumor cell neutralization and transplantation rejection. High levels of specific lymphocyte cytotoxicity were observed by day 7 f0llowing FLV infection; this reactivity reached a peak between 17 and 21 days, and returned to background levels by day 36. Further, positive Winn assays were obtained with spleen cells from mice immunized with FLV at times when the mice resisted live FBL-3 tumor challenge. Positive lymphocyte transformation was obtained with spleen cells from mice immunized with FLV or FBL-3, but not with cells from normal mice or mice immune to a syngeneic methycholanthrene-induced tumor, when cultured with papain-soluble FBL-3 or RBL-5 tumor-cell extracts or mitomycin-C (MMC)-treated FBL-3 or RBL-5 cells. Positive reactivity in the lymphocyte transformation assay occurred after reactivity had peaked in the lymphocyte cytotoxicity test. Similar positive macrophage migration inhibition patterns were also obtained with peritoneal exudate cells (PEC) from FLV-immunized mice using papain-solubilized tumor-associated antigen (TAA) from FBL-3 cells. These data suggest that sequential development and modulation of CMI reactivity occurs as observed in different assays following immunization in this system.
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PMID:Cellular immune reactivity in vitro and tumor rejection provided by tumor-associated antigens of friend-virus-induced leukemia. 118 39

The Mr 55,000 interleukin 2 receptor peptide (Tac; CD25) is not expressed by normal resting T-cells but is markedly up-regulated in adult T-cell leukemia and other malignancies, as well as on T-cells activated in normal immune, autoimmune, allograft, and graft-versus-host settings. Anti-Tac is a mouse monoclonal antibody directed against the Tac peptide. Our prior attempts to use this antibody in humans for antitumor therapy and immune regulation have been limited by weak recruitment of effector functions and neutralization by antibodies to mouse immunoglobulins. To circumvent these difficulties, we prepared several chimeric "humanized" anti-Tac antibodies by genetic engineering, including one "hyperchimeric" antibody (anti-Tac-II) in which the molecule is human except for the small hypervariable segments of the complementarity-determining regions retained from the mouse antibody. These constructs maintain high affinities for antigen and abilities to block T-cell activation and demonstrate new capabilities to perform antibody-dependent cell-mediated cytotoxicity, absent in the mouse anti-Tac. Hence, humanized antibodies have been developed to a tumor-associated antigen and activated T-cell marker with significant features that offer new therapeutic possibilities for select neoplastic and immune disorders.
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PMID:Anti-Tac-H, a humanized antibody to the interleukin 2 receptor with new features for immunotherapy in malignant and immune disorders. 240 13

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

Twenty-four, six month old lambs were assembled into four groups of five animals each and one group of four animals. All groups were inoculated with lymphocytes from a single donor lamb infected with bovine leukemia virus. The inoculum varied from 250 to 250,000 lymphocytes, in tenfold increments. Animals were exposed by intradermal injection in the neck region immediately anterior to the left shoulder joint. All groups were monitored at 0, 3, 7 and 12 weeks after inoculation using the following procedures: a. Syncytia induction assay for detection of bovine leukemia virus in peripheral blood lymphocytes. b. Agar gel immunodiffusion against the gp51 antigen of bovine leukemia virus for the detection of antibovine leukemia virus gp51 antibody. c. Lymphocyte stimulation test for the assessment of cell-mediated immunity using mitogen, nonfractionated bovine leukemia virus antigen, and partially purified bovine lymphoma tumor-associated antigen for the in vitro activation of lymphocytes from bovine leukemia virus-inoculated and sham-inoculated, control animals. d. Routine hematological techniques for the assessment of total leukocyte and lymphocyte counts. The median infectious dose for lymphocytes from the single bovine leukemia virus-infected donor used in this study was determined to be 2000 cells. The syncytia induction assay detected more infected individuals (13/23) at an earlier time than did the agar gel immunodiffusion assay (10/23). Using either serological or virus isolation techniques, infected animals were first detected at three weeks postinoculation in the group receiving the high-dose inoculum and at seven weeks postinoculation in groups receiving low- or medium-dose inocula.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of virus dose in experimental bovine leukemia virus infection in sheep. 283 45

We investigated the intracellular cyclic AMP (cAMP) level and cytotoxic sensitivity to anti-tumor-associated antigen (anti-TAA) antibody in transplantable rat fibrosarcoma cells with regard to each of three days following ip transplantation. The cytotoxic sensitivity of the 3-methylcholanthrene (MCA)-induced transplantable fibrosarcoma KMT-17 cells to anti-TAA antibody decreased daily after ip transplantation in syngeneic WKA/Hok rats. In contrast, the intracellular cAMP level of the tumor cells increased daily after ip transplantation, and the cAMP level of 3-day-old KMT-17 tumor cells (1.31 pmol/10(6) cells) was statistically (p less than 0.01) higher than that of 1-day-old tumor cells (1.01 pmol/10(6) cells). This phenomenon disappeared, however, after artificial infection of the tumor cells with Friend murine leukemia virus (F-MuLV). The cytotoxic sensitivity of F-MuLV-infected KMT-17 (FV-KMT-17) tumor cells to anti-TAA antibody did not decrease and no elevation of the intracellular cAMP level was observed (0.92-0.97 pmol/10(6) cells), regardless of the number of days after ip transplantation. The cytotoxic sensitivity of KMT-17 and FV-KMT-17 tumor cells to anti-TAA antibody was therefore in inverse proportion to the intracellular cAMP levels of the tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Correlation between intracellular cyclic AMP level and cytotoxic sensitivity to anti-tumor-associated antigen antibody in rat fibrosarcoma cells]. 285 17

Low tumor-associated antigen (TAA) expressing tumor cells present an obstacle to effective antibody directed purging of tumor cells from bone marrow. In this study, a comparison was made of the efficiency with which low TAA expressing leukemia cells could be depleted using two monoclonal antibody (MoAb) directed purging techniques: 1) complement (C)-mediated cytolysis, and 2) physical separation using magnetic microspheres. Low TAA sublines were selected from a cultured human leukemia cell line by growing out cells remaining after treatment with anti-TAA and C, or after immunomagnetic (IM) purging. IM-selected sublines showed lower TAA expression than did C-selected sublines, and sublines resulting from multiple selections expressed less TAA than those that had only been through one selection. These sublines were then examined for sensitivity to C or IM purging. The highly selected, lowest TAA expressing sublines were markedly resistant to both IM and C. Less selected sublines were resistant to C, but not to IM. In both techniques, addition of MoAbs against a second TAA restored the efficiency of purging to that observed with the parental line. When low TAA subline cells were seeded into simulated bone marrow and subjected to purging, C-mediated lysis removed less than 40% of leukemia cells, whereas IM purging removed 85% of the cells. These results indicate that there are low antigen density cells that are resistant to C-mediated purging, but which retain sensitivity to IM removal.
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PMID:Low antigen density leukemia cells: selection and comparative resistance to antibody-mediated marrow purging. 291 23


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