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)

We have presented the rationale for the in vitro approaches that we have taken for generating cytotoxic lymphocytes capable of lysing autologous leukemia cells or leukemia cells from HLA identical siblings. Two different approaches have been used, both of which are based on earlier findings concerning the antigenic and cellular interactions involved in the generation of strong cytotoxic responses to alloantigens in mixed leukocyte culture.
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PMID:Elicitation of anti-leukemia cytotoxic responses. 16 56

A serially progagated cell line (L104) was established by co-cultivation of alung adenocarcinoma (L-1) from a patient with concurrent chronic lymphocytic leukemia and XC, a non-producer rat line, known to carry the Rous sarcoma virus (RSV) genome. Karyotype of the L104 cultures revealed predominantly rat-like patterns; however, about 5% of the cells reacted with HLA antibodies and demonstrated human isozyme patterns. Electron microscopy of L104 cells revealed the presence of C-type particles budding from the cell membranes and in cytoplasmic vacuoles. Virus was not detected in any of the other normal lung, lung tumor or XC cells examined after co-cultivation with XC cells. The particles isolated from tissue culture fluids had the biochemical and biophysical characteristics common to other known mammalian C-type particles and were serologically related to the woolly monkey virus (WMV)/gibbon ape leukemia virus (GaLV) complex. Cross-hybridization between viral 3H-DNA transcripts and cellular RNAs from virus-infected cells clearly show the presence of sequences in the L104 cellular RNA related to both the GaLV/WMV group of viruses and rat viruses. Hydroxyapatite chromatography reveals however that the primate-related sequences in the viral RNA are indistinguishable from WMV in thermal elution profile. The host range of L104 virus appears to vary greatly from WMV in being xenotropic and, in the cell lines thus far tested appears, to infect only rat cells. The virus gave positive KC but negative XC assays. Inoculation of whole cells or cell-free supernatants into weaning hamster did not result in either solid tumors or leukemia. Co-cultivation of appropriate cell lines may represent an approach to the detection of latent viruses in human neoplasia.
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PMID:Appearance of C-type virus-like particles after co-cultivation of a human tumor-cell line with rat (XC) cells. 17 Feb 17

Virion antigens of feline leukemia virus are associated with HLA antigens in the membrane of human cells infected with the virus. Feline leukemia virus produced by these cells incorporates host membrane antigens into the virion envelope, making the virus susceptible to lysis by antisera directed to HLA or to uninfected cells plus complement.
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PMID:Incorporation of HLA antigens into the envelope of RNA tumor viruses grown in human cells. 22 20

Cytotoxic antibodies to antigens specific for leukaemic myeloblasts have been sought in the serum of patients with acute myeloblastic leukaemia treated by immunotherapy with irradiated allogeneic myeloblasts and BCG. Assays of complement- and K-cell-mediated activity were used. Cytotoxicity to allogeneic myeloblasts was detected in both assays. When sera from 15 patients, taken at various times during immunotherapy, were systematically tested against a panel of 5 myeloblasts, the following patterns emerged: 1. No antibody was cytotoxic against all myeloblasts of the panel in either the K-cell or complement-dependent assay. However, all myeloblasts of the panel were lysed by a number of sera. 2. Cytotoxic antibody was detected as often against a panel of lymphocytes from healthy donors as against the panel of allogeneic myeloblasts. 3. Fresh and cryopreserved myeloblasts were equally susceptible to lysis in both assays. 4. Experiments failed to demonstrate any deterioration of cytotoxic antibody on storage. 5. The number of K-cell-revealed cytotoxic antisera increased with length of immunotherapy. This pattern was not apparent for antibodies revealed by complement. 6. No instance of cytotoxicity in either assay was seen when serum was tested against 12 autologous myeloblasts. It is considered that cytotoxic antibody detected with allogeneic myeloblasts is probably directed against HLA antigens common to immunizing and test target myeloblasts and target lymphocytes.
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PMID:Cytotoxic antibody in acute myeloblastic leukaemia during immunotherapy: lack of tumour specificity. 26 30

Several laboratories have recently observed that common HLA typing sera contain antibodies to various nonHLA antigens, including leukemia-associated antigens and normal platelet, granulocyte, or B-lymphocyte-specific alloantigens. In order to study the possible effects of these antibodies on HLA typing data in leukemia, several of these sera were adsorbed with HLA typed platelets, purified B-lymphocytes, cultured lymphoblasts, or mononuclear cells from patients with active leukemia of various types, and retested for residual activity against previously reacting cells. The results indicate that many of the reactions of leukemia cells to HLA typing sera represent reactions to nonHLA antibodies, many of which are directed against antigens common to cultured lymphoblasts, leukemia cells of several types, and normal B-cells. In the absence of family studies or prior serum adsorption, caution should be used in interpretation of all data related to HLA antigens in leukemia.
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PMID:HLA typing of leukemic cells and lymphoblastoid cell lines: effects of non-HLA antibodies in common typing sera. 26 54

Selective adsorption of several common "monospecific" HLA typing sera with HLA typed platelets, purified B lymphocytes, cultured lymphoid cells, or lymphocytes from patients with active chronic lymphocytic leukemia demonstrated that many of these sera contain antibodies to non-HLA antigens. Antibodies were detected to antigens present on peripheral blood B-lymphocytes, cultured lymphoid cells and leukemic cells from patients with both myelocytic and lymphocytic forms of leukemia but absent from T-lymphocytes and platelets. Since these kinds of antibodies appear to be present in a large proportion of common HLA typing sera, caution should be used in interpreting all data related to HLA antigen expression in leukemia.
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PMID:Possible effects of non-HLA antibodies in common typing sera on HLA antigen frequency data in leukemia. 30 30

Acute lymphocytic leukemia developed almost simultaneously in two adolescent brothers, and another brother and both parents had rheumatoid arthritis. Laboratory studies uncovered no evidence for an underlying immunodeficiency state in the family. Immunogenetic evaluation showed the leukemic siblings to be HLA- and mixed-leukocyte-culture identical and homozygous for a recessively inherited locus dictating the presence of antigens on the surface of B-cells. This Ia antigen, as detected by sera from mothers of leukemic children, appeared to be mapped within the major histocompatibility region and may be a human analogue to murine immune-response antigens associated with susceptibility to leukemia.
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PMID:Immunogenetic determinants of familial acute lymphocytic leukemia. 30 33

Cold non-HLA lymphocyte cytotoxins were found to be principally reactive against B lymphocytes. These antibodies were studied in 1335 patients with a wide range of diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), scleroderma, Hashimoto's disease, asthma, diabetes, lymphoma, psoriasis, leukemia, multiple sclerosis, and also in healthy donors. Antibodies reactive to B lymphocytes in the cold or warm test conditions were not directed against HLA specificities. Since B lymphocytes differ from T lymphocytes principally in that they have surface immunoglobulin, it is postulated that at least one target antigen of cold lymphocyte cytotoxins is not a virus, infectious agent, or a genetically determined structural antigen, but, rather, simply immunoglobulin.
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PMID:Non-HLA lymphocyte cytotoxins in various diseases. 31 13

Based on the presence or absence of erythrocyte receptors(E) a T cell marker, acute lymphocytic leukemia (ALL), can be divided into E+ALL and E-ALL. We studied cell surface antigens on blasts from 12 children with untreated ALL: eight with E-ALL and four with E+ALL. Heterologous antisera were raised against thymus cells, E+ and E-ALL blasts, appropriately absorbed and tested by immunofluorescence and a radiolabeled antibody assay with normal and leukemic lymphoid cells. By both methods, anti-thymus and anti-E+ALL sera reacted with human thymocytes. Specific binding of anti-E+ALL serum to T antigens was indicated by the fact that a single absorption with thymocytes abolished its binding to allogenic thymocytes, and the reactivity of anti-E+ALL serum with thymus, blood and bone marrow lymphocytes was similar to that of anti-thymus serum. After exhaustive absorption with blood leukocytes, anti-E+ALL and E-ALL sera were negative against normal lymphocytes and bone marrow cells from children with ALL in remission. Anti-thymus and anti-E+ALL sera reacted with blasts from patients with E+ALL, but not with E-ALL. In contrast, anti-E+ALL serum reacted with 40 to 96% of blasts from all children with E-ALL, whereas of the four patients with E+ALL, two were negative and two had the lowest percentage of immunofluorescent cells (10 to 22%). These results were confirmed with the radiolabeled antibody assay. Patients with active E-ALL had cells bearing E-ALL antigen(s) in the peripheral blood and bone marrow, but the number of immunofluorescent cells was lower in blood. Cells reactive with anti-E-ALL serum did not react with thymus cells, blood lymphocytes, remission bone marrow cells, Raji cells, PWM and PHA-induced blasts and CLL cells bearing mIg (uk). These data suggest that the antigen detected on E-ALL blasts by anti-E-ALL serum is neither a HLA-related nor a cell differentiation antigen. Thus, by using antiserum to E+ALL blasts, we have confirmed the presence of a T cell-specific antigen(s) on E+ALL cells. This antiserum did not recognize other leukemia-associated antigens common to E+ and E-ALL. We have also demonstrated an antigen(s) which is regularly expressed on E-ALL blasts and is either not detectable or is present in a lower proportion of E+ALL blasts.
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PMID:Acute lymphoblastic leukemia (ALL) antigens detected with antisera to E rosette-froming and non-E rosette-forming ALL blasts. 31 69

Fourteen patients with chronic granulocytic leukemia received bone marrow grafts from HLA identical siblings. Ten patients were in blast crisis prior to grafting, three were in an accelerated phase of their disease, and one was aplastic secondary to chemotherapy. Prior to transplant all patients were conditioned with chemotherapy including cyclophosphamide plus 1,000 rad of total body irradiation. Ten patients achieved engraftment while four died 1 to 26 days after marrow infusion without functioning grafts. Two patients received a second infusion of donor marrow because of delayed engraftment. Neither marrow cell dose nor presence of myelofibrosis correlated with successful engraftment. Three out of ten engrafted patients developed graft-versus-host disease. Interstitial pneumonia occurred in seven patients. The immediate cause of death was bacterial septicemia in six patients. All evidence of leukemia disappeared in nine out of ten evaluable patients. The median survival was 43 days. One patient had a complete remission of 16 months duration.
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PMID:Treatment of chronic granulocytic leukemia by chemotherapy, total body irradiation and allogeneic bone marrow transplantation. 36 30


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