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)

Serum thiobarbituric acid (TBA) reactivity for lipoperoxidation products was assessed at diagnosis in children with T-cell and common acute lymphocytic leukemia (ALL) and T-lymphoblastic lymphoma. Comparisons were made among these groups and with healthy controls. Mean TBA reactivity (mumol malondialdehyde/L serum) was increased (P less than 0.01) in the T-cell leukemia group versus common ALL and T-lymphoblastic lymphoma patients and controls, respectively. The increase in lipoperoxidation products in T-cell ALL appeared to bear a positive relation to peripheral leukocyte counts, and was accompanied by increased serum prostaglandin E2 (PGE2) levels in most representative cases. Indomethacin added to a childhood T-cell ALL line (SUP-T3), at a concentration known to inhibit prostaglandin synthesis in vitro (i.e., 3 micrograms/mL), effected significant increases in the numbers of natural killer (NK; Leu-11+ and Leu-19+) cells (P less than 0.01) and B-lymphocytes (P less than 0.05), and significant decreases in cell viability (P less than 0.01). Indomethacin may be a useful agent for enhancing the antileukemic immune response in T-cell ALL.
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PMID:Lipoperoxidation and T-cell leukemia of childhood. Effects of indomethacin. 280 98

The incorporations of [3H] thymidine, [3H]uridine and [3H]leucine into DNA, RNA and protein synthesis in leukemia 7712 cells were inhibited by the complex of 3,6-di-(dimethylamino)-dibenzopyriodonium with praseodymium (Pr, rare earth element) dicitrite 34 micrograms/ml for 3-24 h. The degree of inhibition increased in proportion to the incubation time. After being treated with [C17H20N2I]3[Pr(C6H5O7)2] 34 micrograms/ml for 3, 6, 12 and 24 h, the incorporation of [32P]Na2HPO4 into the nucleoprotein of leukemia 7712 cells was inhibited by 49, 57, 65 and 85%, while those into ATP were inhibited by 43, 59, 65 and 83%, respectively. The ID50 of [C17H20N2I]3[Pr(C6H5O7)2] on DNA synthesis in leukemia 7712 cells at 24 h was 22 micrograms/ml. After the complex was removed from the medium entirely, the rate of DNA synthesis decreased with time over 3-12 h. This result indicated that the inhibition mechanism was likely due to damage to the DNA template.
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PMID:[Effects of complex of 3,6-di-(dimethylamino)-dibenzopyriodonium with praseodymium dicitrate on the syntheses of DNA, RNA, protein, nucleoprotein and ATP of leukemia L 7712 cells in mice]. 281 22

The p35 protein which is hyperexpressed on hairy leukemic cells was determined to be Ii, the electrophoretically invariant glycoprotein that is associated with class II major histocompatibility complex (Ia) antigens from the time of their synthesis. The principal function of class II MHC antigens is to present to T cell receptors those digested foreign antigenic peptides that probably fold as amphipathic alpha-helices and adsorb to a hydrophobic surface (desetope) on Ia. By a novel strip-of-helix hydrophobicity algorithm we found that the sequence Leu-142 to His-170 in Ii formed a five-cycle, amphipathic, alpha-helix, the highest scoring one among a series of proteins commonly used as experimental antigens. This finding led to the hypothesis that this sequence in Ii bound to the antigen-binding site (desetope) of Ia until release and self-aggregation in the endosome in order that digested foreign peptides could then bind to Ia. Abundant expression of Ii in leukemic cells might be associated with an altered capacity of those cells to present foreign or leukemic antigens to the host's immune system.
Leukemia 1987 Apr
PMID:Hyperexpressed hairy leukemic cell Ii might bind to the antigen-presenting site of class II MHC molecules. 282 17

Selective in vitro photodestruction of HPB-ALL human T-cell leukemia cells was accomplished using the photosensitizer chlorin e6 coupled through dextran molecules to an anti-T-cell monoclonal antibody (mAb), anti-Leu-1. Conjugates with mAb/chlorin molar ratios as high as 1:36 retained mAb binding activity, and the absorption spectrum and quantum efficiency for singlet oxygen production of bound chlorin (0.7 +/- 0.2) were unchanged from that of the free photosensitizer. Phototoxicity, as measured by a clonogenic assay and by uptake of ethidium bromide, was dependent on the doses of both mAb-chlorin and 630- to 670-nm light, was enhanced by 2H2O, and was observed only in target populations that bound the mAb. Similarly, free chlorin e6 in solution had no photodynamic effect in amounts 100 times more than that carried by the mAb. For this antibody-targeted system, approximately 10(10) molecules of singlet oxygen were necessary to kill a cell.
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PMID:Antibody-targeted photolysis: selective photodestruction of human T-cell leukemia cells using monoclonal antibody-chlorin e6 conjugates. 287 61

Cells from two patients with primary mediastinal tumors of clear cell type were characterized by immunological and molecular biological techniques. In both cases a B cell immunophenotype was suggested by the positive staining for the B1 (CD20), B4 (CD19), Leu 14 (CD22), as well as staining with other B monoclonal antibodies by immunohistochemistry. However, no definitive evidence for the expression of Ig light or heavy chains at the protein level was found. Southern blot analysis of Ig heavy and light chain gene rearrangements revealed clonal B cell populations in both cases. There was no indication of a somatic joining of T cell receptor (TCR) genes using probes for TCR beta and or TCR gamma genes. Thus, our results suggest a clonal B cell origin of clear cell lymphomas in the mediastinum.
Leukemia 1989 Feb
PMID:Clonal immunoglobulin gene rearrangements in primary mediastinal clear cell lymphomas. 291 Dec 6

To determine the utility of tissue section immunochemistry in the evaluation of bone marrow involved by lymphoid and plasma cell malignancies, snap-frozen, undecalcified bone marrow core and aspirate samples from 23 patients with these disorders were studied with a battery of monoclonal antibodies. With techniques that preserve architecture, difficult diagnostic cases characterized by core but not aspirate involvement, or the reverse, were resolved. By means of an extensive battery of monoclonal antibodies applied to serial sections, complex tumor cell phenotypes were established in all 23 cases. In addition to the identification of straightforward monoclonal surface immunoglobulin expression in small cleaved cell lymphomas (four cases), the battery approach added immunologic certainty in malignancies with unusual or difficult phenotypes: peripheral T-cell lymphomas with idiosyncratic antigen expression, and chronic lymphocytic leukemias and small cell lymphomas with faint surface immunoglobulin expression (four cases). For the chronic lymphocytic leukemias and the small cell lymphomas, the combined IgD+, B2+, B1+, Ia+, Leu-1+ phenotype taken as a whole had greater utility than any isolated marker. The acute lymphocytic leukemias and the myelomas studied demonstrate the wide range of B-cell antigens that must be detected to account for the variety of B-cell neoplasms encountered. Additionally, the previously undescribed phenotypic subset of CALLA+ myelomas, which is of prognostic relevance, was identified. Marrow frozen section immunotyping is a major asset in the evaluation of patients with lymphoma, leukemia, and myeloma when special care is accorded to tissue handling and to treatment of endogenous peroxidase/pseudoperoxidase and interstitial immunoglobulin.
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PMID:Immunotopographic assessment of lymphoid and plasma cell malignancies in the bone marrow. 293 17

Important insights into leukocyte differentiation and the cellular origins of leukemia and lymphoma have been gained through the use of monoclonal antibodies that define cell surface antigens and molecular probes that identify immunoglobulin and T cell receptor genes. Results of these studies have been combined with markers such as surface membrane and cytoplasmic immunoglobulin on B lymphocytes, sheep erythrocyte receptors on T lymphocytes, and cytochemical stains. Using all of the above markers, it is now clear that acute lymphoblastic leukemia (ALL) is heterogeneous. Furthermore, monoclonal antibodies that identify B cells, such as the anti-B1 and anti-B4 antibodies in combination with studies of immunoglobulin gene rearrangement, have demonstrated that virtually all cases of non-T-ALL are malignancies of B cell origin. At least six distinct subgroups of non-T-ALL can now be identified. T-ALL is subdivided by the anti-Leu-9, anti-Leu-1, and antibodies that separate T lymphocyte subsets into three primary subgroups. Monoclonal antibodies are also useful in the subclassification of non-Hodgkin's lymphoma, and certain distinct markers can be correlated with morphologic classification. The cellular origin of the malignant Reed-Sternberg cell in Hodgkin's disease remains uncertain. A substantial number of investigators favor a myelocyte/macrophage origin based on cytochemical staining; however, consistent reactivity with antimonocyte reagents has not been demonstrated. Although monoclonal antibodies are useful in distinguishing acute myeloid from acute lymphoid leukemias, they have less certain utility in the subclassification of acute myelogenous leukemia (AML). Attempts to subclassify AML by differentiation-associated antigens rather than by the French-American-British (FAB) classification are underway in order to document the potential prognostic utility of surface markers. Therapeutic trials using monoclonal antibodies in leukemia and lymphoma have been reported. Intravenous (IV) infusion of unlabeled antibodies is the most widely used method; transient responses have been demonstrated. Antibodies conjugated to radionuclides have been quite successful in localizing tumors of less than 1 cm in some studies. Therapy trials with antibodies conjugated to isotopes, toxins, and drugs are currently planned. Purging of autologous bone marrow with monoclonal antibodies and complement in vitro has been used in ALL and non-Hodgkin's lymphoma; preliminary data suggest that this approach may be an effective therapy and may circumvent many of the obstacles and toxicities associated with in vivo monoclonal antibody infusion.
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PMID:Immunologic classification of leukemia and lymphoma. 294 Oct 82

T- and B-cell function after autologous bone marrow transplantation (ABMT) was assessed and compared with that found after allogeneic BMT and after chemotherapy only. In all 16 patients with acute leukaemia in remission treated with high-dose chemotherapy and single or double ABMT, T-helper numbers and function in an assay measuring PWM-induced Ig synthesis were grossly defective and closely resembled the defects observed after allo-BMT involving chemoradiotherapy (six patients). T-helper activity was more variable after chemotherapy only (eight patients), but in individual patients the defect was as great as that observed after BMT. In contrast, suppressor activity was comparably increased in all patient groups and increased numbers of Leu 15+ Dr+ Tac- suppressor T cells were consistently observed, suggesting chronic activation of suppressor T cells, the cause of which remains unknown. B-cell function was also uniformly impaired in all patients tested. It is therefore concluded that defective immune function after BMT is not due to alloimmune or radiotherapy-mediated effects. Furthermore, since many patients were studied a prolonged period after BMT and had no T cells with a thymic phenotype and no evidence of infection, it is unlikely that the defects are secondary to cellular immaturity following marrow regeneration or to superadded infection. The gross immune defects observed after various forms of BMT are likely, therefore, to be directly attributable to the chemotherapy involved.
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PMID:Lymphocyte function after autologous bone marrow transplantation (BMT): a comparison with patients treated with allogeneic BMT and with chemotherapy only. 294 70

A 27-year-old male patient with ataxia telangiectasia (AT) developed atypical chronic lymphocytic leukemia with increasing bone marrow infiltration in the absence of organomegaly. One-third of the leukemia cells expressed a mature suppressor/cytotoxic T cell phenotype (T3+ T4- T6- T8+ T10-), two-thirds demonstrated additional helper/inducer T cell-associated antigens (T3+ T4+ T6- T8+ T10-), and a small fraction reacted with a natural killer (NK) cell-specific monoclonal antibody (Leu 11+). The proliferative response to stimulation in vitro with lectins and various monoclonal antibodies resembled the proliferation pattern of mature thymocytes: The cells responded to phytohemagglutinin (PHA), concanavalin A (ConA), stimulation of the T3-Ti receptor complex with Sepharose-bound anti-T3, and stimulation of the sheep erythrocyte receptor protein with anti-T11(2) and anti-T11(3) in conjunction with exogenous interleukin-2 (IL 2); they failed, however, to proliferate after stimulation with anti-T11(2) and anti-T11(3) alone. There was no response in the mixed lymphocyte reaction (MLR) and no suppression of the MLR between two healthy donors. Antibody-dependent cell-mediated cytotoxicity and NK activity could not be demonstrated. Cytogenetic analysis revealed complex clonal aberrations, including an interstitial deletion of the long arm of chromosome 14 concerning bands q21-31, loss of chromosome 20, and loss of the Y chromosome. Cytostatic chemotherapy was of little use and caused serious side effects, whereas leukapheresis proved effective in reducing the tumor load. The clinical data and laboratory findings in this case correspond to three previously described patients with AT who developed chronic T cell leukemia. Thus, in adult patients with AT, malignant proliferation of cytogenetically marked and phenotypically heterogeneous mature T cells seems to be a frequent complication.
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PMID:Chronic T cell leukemia with unusual cellular characteristics in ataxia telangiectasia. 294

Rat basophilic leukaemia (RBL) cells are known to possess three different kinds of receptors capable of interacting with IgE, which have been named R, H and 71K and which differ in apparent molecular weight (MW) as determined by SDS-PAGE. Reduction of receptors isolated from surface-iodinated RBL cells reduced the MW of 71K to a value corresponding to the MW of R without altering significantly the MW of H or R. Only a single reduction product of 71K could be detected when either surface-iodinated or 3H-leucine labelled RBL cells were used. Analysis of one- and two-dimensional tryptic peptide maps derived from surface-iodinated receptors revealed a similarity between R and 71K. The tryptic peptides of H exhibited an entirely different pattern. These results suggest that 71K consists either of two disulphide-linked R-like molecules, or of one such molecule linked to another as yet undetected polypeptide chain.
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PMID:Disulphide-linked receptors for IgE on rat basophilic leukaemia cells. 294 66


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