Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ICO-G-2 hybridoma clone was obtained after fusion of spleen cells from BALB/c mice immunized with cells from a patient with acute myelomonoblastic leukemia (AMML) and P3 X 63 Ag8.653 cells, using 50% polyethyleneglycol, molecular weight 1500 KD. The antigen with a molecular weight of 100 KD was present only on polymorphonuclear neutrophils and eosinophils of the peripheral blood. The antigen expression was also found on the majority of myeloid precursors and some nuclear erythroid cells. CFU-GM did not express the antigen. Monoclonal antibodies ICO-G-2 reacted with blast cells of some patients with AML, AMML and CML. The antibodies did not react with cells from patients with AMonL, CMonL, ALL, CLL and LSA. Such pattern of reactivity makes these monoclonal antibodies useful for the differential diagnosis of acute nonlymphocytic leukemias and CML in blast crisis.
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PMID:[Monoclonal antibodies to the antigen of myeloid cells]. 362 Jun 54

A MCA raised against the human acute myelogenous leukaemia cell line KG1 reacted with only KG1 among 26 haematopoietic cell lines covering the major lineages. It reacted with early myeloid (M1/2), 1 of 2 acute myelomonocytic (M4) and most non-B non-T leukaemias, including blast crises of CGL. Among M1-AML cells, both MPO+ and MPO- blasts were BI-3C5+. Blasts in 3 Tdt+ M1-AMLs were simultaneously BI-3C5+. BI-3C5 reacted with 4% cells in normal BM, many of which were histologically recognisable as myeloid precursors. 8-15% of BI-3C5+ cells in BM were simultaneously Tdt+, and all were weakly Ia antigen+. BI-3C5 was unreactive with all peripheral leucocytes, with M3 and M5 AMLs, with lymphoid and myeloid leukaemias of "mature" phenotype (T-ALL, B-ALL, CLL, CGL) and with non-haematopoietic cell lines. BI-3C5 precipitated a 120K moiety from 125I-labelled KG1 membranes. It was not blocked by J5 anti-cALLA. The potential use of BI-3C5 in the classification of acute leukaemias is discussed.
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PMID:A novel monoclonal antibody BI-3C5 recognises myeloblasts and non-B non-T lymphoblasts in acute leukaemias and CGL blast crises, and reacts with immature cells in normal bone marrow. 385 2

Total cellular RNA from a series of leukemic cell populations, both myeloid and lymphoid, as well as from normal circulating lymphocytes was analysed for the expression of two cellular oncogenes, c-myc and c-myb, by Northern blot hybridization assay. Expression of c-myc but not of c-myb was observed in unstimulated normal lymphocytes. Stimulation by PHA was shown to activate the expression of both genes. Remarkably different levels of expression of c-myc were observed in ALL, whereas in CLL the expression of c-myc was uniformly low or absent. Differential expression of c-myc was detected in AML as well as in CML, c-myb was differentially expressed in AML and ALL, and absent in CLL and CML. Other single cases of hemopoietic disorders were studied, but the expression of the two oncogenes was low or absent. Neither evident genome amplification nor genome rearrangements were detected in the cell DNAs digested with restriction endonucleases.
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PMID:Study of the levels of expression of two oncogenes, c-myc and c-myb, in acute and chronic leukemias of both lymphoid and myeloid lineage. 386 Jun 96

The rat monoclonal antibody CAMPATH-1 recognizes a hitherto undefined antigen present on virtually all normal lymphocytes and monocytes. Its reactivity with 105 samples of fresh leukaemic cells and 13 cell lines was measured by indirect fluorescence and peroxidase staining to define in more detail which stages of differentiation it recognizes. It was found to bind to cells from virtually all cases of lymphoid leukaemia (B cell CLL, T cell ALL, cALL and the few examples of HCL, PLL, Sezary syndrome and CGL in lymphoid blast crisis). The single case of cALL in relapse and four of six cases of null ALL were negative. Binding to non-lymphoid leukaemia cells (AML, AMML, AMoL, APL, AEL and CGL in blast crisis) was weaker or undetectable. Binding to established lymphoid cell lines was generally weak compared with fresh cells but some lines (MOLT4, DAUDI and X308) expressed adequate amounts of antigen to be lysed by CAMPATH-1 with human complement. Because CAMPATH-1 is very effective at killing lymphocytes in the presence of human complement, it has been used for removal of T cells in allogeneic transplants. The present results suggest that it might also have a role in purging bone marrow of leukaemia cells prior to autologous transplantation for acute lymphocytic leukaemia.
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PMID:Reactivity of rat monoclonal antibody CAMPATH-1 with human leukaemia cells and its possible application for autologous bone marrow transplantation. 389 Sep 29

Redistribution and the ability for removing immunological complexes in CLL and CGL cells treated with the specific anti-leukemia antigens were investigated. The immunofluorescence method at 4 and 37 degrees C was applied at different times of cell incubation with antigens. It was shown, that incubation at 4 degrees C even carried out for 18 h, neither caused a clear aggregation nor a release of immunological complexes from the leukemia cell surface, whereas at 37 degrees C considerable differences in mobility of CLL and CGL cells were observed. In CGL cells quite a rapid redistribution followed by the removal of antigen-antibody complexes was observed, while CLL cells have shown the ability for aggregation only, without clear polarization and without releasing the formed complex from the cell surface.
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PMID:Antibody-dependent redistribution and release of immunological complexes in cells of human chronic leukemias. 615 21

Serological analysis of human membrane antigens have been performed using rabbit xenosera against membrane fraction obtained from different cells (B cell lines: RAJI, RAMOS, DAUDI, UHKT-2: T cell line: MOLT-3, as well as normal pooled lymphocytes). The direct cytotoxicity testing demonstrated that xenogeneic rabbit B lymphoid antisera mediated a significant reaction in the complement-dependent cytotoxicity assay against an antigenic determinant on normal peripheral blood B lymphocytes but not against T lymphocytes and granulocytes. Moreover, these xenoantisera react with antigenic specificities present on the CLL leukocytes, on some AML myeloblasts, on the hairy cells, on majority of ALL and CML blasts, but not on eosinophilic leukocytes and on T lymphocytes from peripheral blood of patients with CLL, ALL, AML, and CML in remission. These xenoantisera react with antigenic specificities present on the cells of cultured lymphoid cell lines of B type, but not on cells of T cell lines.
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PMID:Reaction of various human normal and leukemic cells and cells of different cell lines with rabbit antisera prepared against membrane fraction of B and T cell lines. 618 60

The enzyme 5'-nucleotidase (5'-N) was demonstrated cytochemically in blood cells using a modification of the Wachstein and Meisel technique [30]. In peripheral blood the activity was found to be localised mainly in the cell membrane of lymphocytes. A semiquantitative score of 5'-N positivity, was assessed in lymphocytes from eight normal donors and 60 patients with various types of leukaemia and lymphoma. The lymphocyte score of 5'-N was slightly reduced in CML and AML but markedly reduced in most lymphoproliferative states tested. The only supranormal activity was found in two of 18 cases of CLL.
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PMID:5'-Nucleotidase in lymphocytes from various clinical disorders. 630 May 63

Neutrophil myeloperoxidase (MPO) activity was analysed semi-quantitatively both by (i) MPO-scoring of polymorphonuclear leucocytes (PMN) and (ii) counting the MPO-deficient PMN (PMN lacking MPO) in 164 subjects (60 cases of leukaemia and 104 normal humans). The scoring method showed that 10 out of 21 (48%) cases of acute myeloid leukaemia (AML), 2 out of 10 (20%) cases of chronic myeloid leukaemia (CML), 0 out of 29 cases of lymphoid leukaemia (ALL + CLL), and 1 out of 104 normal humans had decreased MPO scores. These figures correlated well with the more simple counting of PMN lacking MPO in the same groups: 8 out of 21 (37%) cases of AML, 6 out of 10 (60%) cases of CML and 0 out of 29 cases of lymphoid leukaemia showing more than 4% PMN lacking MPO. In cases of otherwise unclassifiable acute leukaemia, a decreased MPO score and an increased number of MPO-deficient PMN suggests the diagnosis of AML and not ALL. Counting the number of PMN lacking MPO was found to be a time-saving and even more reliable method than the semiquantitative scoring of MPO activity in PMN.
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PMID:Myeloperoxidase-deficient polymorphonuclear leucocytes. (I) Incidence in untreated myeloid leukaemia, lymphoid leukaemia and normal humans. 630 66

GH, LH, insulin and glucagon patterns were studied in the peripheral leukocytes of normal subjects (granulocytes and lymphocytes separated on a Ficoll-Hypaque gradient) and leukaemic patients (CML, AML, CLL, and ALL), using a double antibody RIA on whole cells. The uptake of 125I-labelled insulin and GH by these cells was also assessed. The results showed that in leukaemia, particularly CLL, ALL and AML, though not in CML, there was a constant reduction in hormone values, plus depressed GH and insulin uptake. The only exceptions were glucagon and insulin in CML, and LH in CLL, since their concentrations were normal or clearly enhanced. The data are seen as an expression of a membrane receptor block extending to several hormones with structural differences (protein, steroid, T3 and T4), capable of altering the ability of leukaemic cells to respond to ordinary factors modulating their differentiation, functional activity, and the expansion of the corresponding stem cell compartment.
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PMID:[Behavior of the principal protein hormones in normal and leukemic leukocytes]. 630 18

A membrane antigen with an apparent specificity to B lymphocytes was detected with immunochemical techniques and its properties were analyzed. Anti-B-CLL serum was raised in a rabbit by immunization with B-cell chronic lymphocytic leukemia (B-CLL) cells. This anti-B-CLL serum was absorbed with erythrocytes, liver homogenate and insolubilized immunoglobulins. After further absorption with T-CLL cells, chronic myelocytic leukemia (CML) cells and acute myelocytic leukemia (AML) cells, the anti-B-CLL serum still reacted with peripheral blood B lymphocytes, B-CLL cells and hairy cell leukemia (HCL) cells. In contrast, no reactivity was seen with peripheral blood T lymphocyte or monocytes, or leukemia cells of non-B cell origin. An immunoprecipitation of radiolabeled cell surface proteins was attempted using the anti-B-CLL serum in the presence of Staphylococcus Aureus Cowan 1 (SaCl), and the precipitates were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). A membrane antigen with an apparent molecular weight of 76,000 daltons (P-76) was immunoprecipitated with the anti-B-CLL serum from the lysates of normal B lymphocyte, B-CLL cells and HCL cells. The antigen (P-76) is not composed of disulfide-linked subunits and has no structural relationship with HLA-DR (Ia-like) antigens or other known antigens. These results suggest that this antigen is B-lymphocyte specific, and favour the B-lymphocyte nature of HCL cells.
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PMID:A human B lymphocyte antigen (P-76) shared by B-cell chronic lymphocytic leukemia cells and hairy cell leukemia cells. 634 Jul 59


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