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)

Phenotypes of cells from 12 patients with acute myelogenous leukemia (AML) were analysed by means of a fluorescence-activated cell sorter utilizing a panel of monoclonal antibodies (MAbs). A majority of the cells from peripheral blood coexpressed the antigens against MAbs CD11, CD13, and CD33 but did not express the antigens against CD1, CD3, CD4, CD5, CD8, CD19, CD20, CD21, CD41 and 42, and glycophorin A. Three out of the 12 cases expressed CD7 antigen. However, one of them showed no reaction with Tp40 MAb, whereas the others showed reaction with Leu9 and T55. The discrepancy of reactivities between Leu9 and Tp40 MAbs prompted us to study the promyelocytic leukemia cell line HL-60, which showed similar reactions against Leu9 and Tp40 MAbs. Leu9, OKT16, and T55 MAbs reacted strongly with HL60 cells, whereas Tp40 MAb, which reacted strongly with T-cell leukemia cell line Jurkat, showed no reaction. The reactivity of Leu9, OKT16, and T55 MAbs with HL-60 cells was completely inhibited after preincubation with aggregated human immunoglobulin G (AHIG), which clearly shows the existence of nonspecific binding between these 3 MAbs and HL-60 cells via Fc gamma R. On the basis of our experiments, we conclude that HL-60 cells bind nonspecifically with Leu9, OKT16, and T55 MAbs via FcRI, and this is suggestive that de novo AML cells probably behave in the same fashion. Hence, we recommend that the utilization of murine IgG2a and IgG3 MAbs should be avoided especially in cell surface analysis of myeloid leukemic cells.
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PMID:CD7 false-positive acute myelogenous leukemia and promyelocytic leukemia cell line HL-60: characterization of CD7 epitopes by four monoclonal antibodies. 171 52

Pretreatment peripheral and/or bone marrow blasts from 14 patients with acute unclassifiable leukemia (AUL) expressing myeloid related cell-surface antigen (CDII) or megakaryocyte-platelet related cell-surface antigen (OKM6), were isolated for further analysis in this study. Among 11 cases of CD11+AUL, despite a lack of myeloperoxidase (MPO) activity, one patient's blasts possessed Auer rod in a basophilic cytoplasm and another one's blasts expressed MPO maintaining the same surface phenotype after 20 months of his clinical course. The blast from 2 cases possessed both myelomonocytic and monocyte-specific antigens on the cell-surface, whereas the remaining nine cases completely lacked monocyte-specific antigen which is detectable by monoclonal antibodies, Mo2, My4 and Leu M3 (CD14). In addition, we revealed the presence of MPO protein in the cytoplasm of 3 cases of AUL patients by cytoplasmic immunofluorescence test utilizing monoclonal antibody (MA1). Following these results, the former was diagnosed as acute myelomonocytic leukemia (AMMoL) and the latter as acute myelogenous leukemia (AML) by immunophenotypic analysis using flow cytometry (FACS IV) and cytoplasmic immunofluorescence test. We have also described three cases of acute megakaryocytic leukemia which were demonstrated by the presence of megakaryocyte-platelet-related cell-surface antigens detected by utilizing flow cytometry and monoclonal antibodies in addition to both the PPO activity which was shown by ultrastructural cytochemistry, and the emergence of differentiation antigens while culturing these leukemic cells. The blast of 1 case possessed both platelet GPIb and GPIIb/IIIa cell-surface antigens detected by 5F1 (CD36), AN51 (CDw42), and J15, P2 and HPL2 (CDw41), respectively, whereas the remaining two cases almont lacked the GPIb cell-surface antigen. Hence, the former was diagnosed as immature (pro) megakaryocytic leukemia and the latter as acute megakaryoblastic leukemia from the viewpoint of immunophenotypic analysis as will be discussed in this article. These leukemic blasts did not express both T-cell lineage antigens which are detectable by monoclonal antibodies, T6 (CD1), T11 (CD2), T3 (CD3), T4 (CD4), T1 (CD5), Tp40, Leu9 (CD7), T8 (CD8), and B-cell lineage antigens which are detectable by monoclonal antibodies, B4 (CD19), B1 (CD20), B2 (CD21) and J5 (CD10).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Flow cytometric analysis of myeloperoxidase negative acute unclassifiable leukemias by monoclonal antibodies. Acute myelogenous and acute megakaryocytic leukemia]. 254 Dec 76

Five antigen systems were defined by the monoclonal antibodies (MoAb) produced against mature T cells. The antigens recognized were grouped into two categories based on the antigen distribution on T cells. (a) Tp 120 [mol. wt 120 kilodaltons (120kD)] and Tp40 (40kD), these are on most peripheral T cells, but not on any other cell lineages, i.e. pan-T antigen. (b) Ts32 (32kD), Ts145 (145kD) and TsA (not determined), these antigens are present only on certain populations of peripheral T cells, i.e., T subset antigen. Among these five, Ts145 and TsA are probably novel T cell antigens. Cell surface phenotypes of leukaemias and lymphomas were typed with these MoAb. Ia like antigen negative, null cell type acute lymphocytic leukaemia (Ia- null ALL) are Tp40+, suggesting that this type of ALL belongs to a T cell lineage. T cell ALL (T-ALL) and lymphoblastic lymphoma (LL) were both Tp40+, Ts32+, TsA+ and a half of the cases were Tp120+, but the expression of Tp40 was stronger on LL cells. Mature T cell (T2) lymphoma and adult T cell leukaemia (ATL) were Tp120+, TsA+, while Tp40 was weakly expressed on only one third of the cases. These MoAb were found to be useful to estimate the origin of various T cell malignancies.
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PMID:Five antigens on human T cells detected by mouse monoclonal antibodies. 633 46