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)

Adenosine deaminase (ADA) activity has been measured in the lymphoblasts of 23 untreated patients with acute lymphoblastic leukemia and related to the presence or absence of immunologic cell surface markers. The mean ADA activity in the acute lymphoblastic leukemia population as a whole was increased fourfold over that in normal lymphocytes. 9 of the 23 patients were classified as thymus-derived (T-) cell acute lymphoblastic leukemia on the basis of erythrocyte rosette positivity; the remaining 14 patients had null-cell leukemia. The mean ADA activity (ADA U/mg protein) of T-cell lymphoblasts (102 U) was 3 times higher than the mean of null lymphoblasts (30 U). This difference is statistically significant (P less than 0.02). Measurement of ADA activity offers a biochemical method of distinguishing between immunological subtypes of lymphoblasts which may be of prognostic and therapeutic value.
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PMID:Correlation of adenosine deaminase activity with cell surface markers in acute lymphoblastic leukemia. 30 13

Adenosine deaminase (ADA) activity has been assessed in lymphoid cells of 23 patients with acute lymphoblastic leukaemia (ALL) in order to attempt a further characterization of ALL cells in addition to the well known cytochemical and immunological T and B lymphoid cell markers. ADA activity did not show any correlation with the immunological characterization of the patients investigated; in fact a wide range of ADA activity was observed with levels ranging from 0 to 32 U in T-ALL patients and nearly similar values (from 1.8 to 36 U) in the group of non T--non B ALL cases. Normal values ranged from 2 to 5 U (mean 2.9 U; s.d. +/- 0.8). Some cytochemical patterns (acid phosphatase and PAS) appeared well correlated with T markers of lymphoid cells, whereas they showed no significant relationship with ADA activity.
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PMID:Adenosine deaminase activity in acute lymphoblastic leukaemia: cytochemical, immunological and clinical correlations. 35 73

Adenosine deaminase (adenosine aminophydrolase, ADA) activity was found to be low in lymphocytes of chronic lymphatic leukaemia (CLL) patients compared to normal lymphocytes. This was determined on 42 controls and 49 CLL patients. The mean activity in normal lymphocytes was found to be 4.35 +/- 3.34 mumol/h/10(8) cells while in CLL cells it was 2.45 +/- 2.54 mumol/h/10(8) cells.
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PMID:Adenosine deaminase (ADA) activity in lymphocytes of normal individuals and patients with chronic lymphatic leukaemia. 87 26

Adenosine deaminase (EC 3.5.4.4., ADA) has been measured in the blast cells of 36 patients with acute lymphoblastic, acute myeloid, chronic myeloid and chronic myeloid blast crisis leukaemia. Particularly high levels were found in acute lymphoblastic and chronic myeloid blast crisis patients. The measurement of ADA may be useful diagnostically in the undifferentiated acute leukaemias and in detecting the early onset of blast crisis in chronic myeloid leukaemia. Possible reasons for the elevation of ADA in malignant cells are discussed.
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PMID:Adenosine deaminase activity in leukaemia. 105 44

Synthesis and biological activities of 12 analogs of N6-benzyladenosine are described. The compounds were prepared by two methods: (1) direct alkylation of adenosine with an appropriately substituted benzyl bromide to give the N1-substituted derivative which was then rearranged in base to give the N6-substituted compound, and (2) by nucleophilic displacement of chlorine in 6-chloropurine ribonucleoside, 6-chloro-2-aminopurine ribonucleoside, and 6-chloro-2-aminopurine with an amine. These analogs were examined for their growth inhibitory effect in cultured leukemic cells and also for their effect on adenosine aminohydrolase activity. N6-p-Nitrobenzyladenosine and its 2'-deoxy analog were competitive inhibitors (K1 65, 22 MUM). The 2-amino-N6-p-nitrobenzyladenine and its ribonucleoside were found to be noncompetitive inhibitors of adenosine aminohydrolase. In cultured L1210 leukemia, 2-amino-6-p-nitrobenzylaminopurine and the corresponding ribonucleoside were better growth inhibitors than N6-benzyladenosine, while N6-p-nitrobenzyladenosine, its 2'-deoxy analog, and N6-p-fluorobenzyladenosine were as active as N6-benzyladenosine.
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PMID:Synthesis and biological activities of some N6-(nitro- and -aminobenzyl)adenosines. 105 53

Maloney murine leukemia virus-based, replication-defective retroviral vectors containing the neomycin resistance gene (neo) were developed to transfer the Escherichia coli ada gene coding for O6-alkylguanine-DNA alkyltransferase, into mammalian cells. To optimize gene transfer and expression, the following promoters were linked to ada: the Maloney murine leukemia virus promoter within the long-terminal repeat, the Rous sarcoma virus promoter, the thymidine kinase promoter, or the human phosphoglycerate kinase promoter. Sequences were transfected into the helper virus-free retroviral packaging psi-2 cell line. Recombinant retroviruses were tested in CCL-1 cells, which, like most murine tissues, have low levels of alkyltransferase and are sensitive to 1,3-bis(2-chloroethyl)nitrosourea (BCNU), and in NIH-3T3 cells, which are BCNU resistant and have high levels of alkyltransferase. Lines infected with each of the four retroviruses were selected for neo expression and found to have intact proviral integration and ada gene expression. Alkyltransferase activity was greatest with retrovirus containing the Rous sarcoma virus-ada gene; infected NIH-3T3 cells had up to 2300 units of alkyltransferase/mg of protein compared with 151 units/mg of protein in control cells, and infected CCL-1 cells had up to 1231 units/mg of protein compared with 33 units/mg of protein in control cells. CCL-1 cells expressing ada were more resistant to BCNU cytotoxicity than were controls. However, NIH-3T3 cells expressing ada were only slightly more resistant to BCNU than controls, possibly because most of the ada protein was cytoplasmic rather than nuclear as suggested by immunohistochemical stain. These studies establish a series of retroviruses containing the bacterial ada gene, which efficiently infect mammalian cells. ada expression increases nitrosourea resistance in cells with low mammalian alkyltransferase activity.
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PMID:Increase in nitrosourea resistance in mammalian cells by retrovirally mediated gene transfer of bacterial O6-alkylguanine-DNA alkyltransferase. 267 54

Adenosine deaminase (ADA) deficiency is associated with a fatal severe combined immunodeficiency. Because most patients do not have a suitable marrow donor, the introduction of a normal ADA gene into the patient's marrow cells is a potentially useful alternative therapy. To identify vectors that provide optimal gene expression in human hematopoietic cells, we investigated retroviral vectors containing the ADA gene under the transcriptional control of the promoter/enhancers of Moloney murine leukemia virus, the simian virus 40 early region, the cytomegalovirus immediate-early gene, the lymphotropic papovavirus, and the human beta-globin gene. ADA expression from these vectors was monitored in the ADA- human histiocytic lymphoma cell line DHL-9, and in the multipotential chronic myeloid leukemia cell line K562. ADA expression in infected K562 cells was also measured after induction of megakaryoblastic differentiation by phorbol ester, and after induction of erythroid differentiation by sodium n-butyrate or hemin. In these hematopoietic cell lines, the vectors that contained ADA controlled by either the Moloney murine leukemia virus promoter (LASN) or the cytomegalovirus promoter (LNCA) expressed ADA at much higher levels than the other vectors tested. Furthermore, in K562 cells infected with LASN and LNCA vectors, induction of terminal differentiation resulted in the same or higher level expression of ADA. These cell lines have permitted the evaluation of transduced gene expression in proliferating and differentiating hematopoietic cells that provide a model for bone marrow-targeted gene therapy.
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PMID:Expression of human adenosine deaminase from various strong promoters after gene transfer into human hematopoietic cell lines. 275 48

Adenosine deaminase (ADA) was assayed in plasma from 14 patients with adult T-cell leukemia (ATL) (eight with acute ATL and six with smoldering or chronic ATL), 20 male family members (ten were anti-ATLA antibody positive and the other ten negative), and 25 normal individuals. ADA activity was uniformly higher in plasma from patients with ATL than normal controls. This enzyme activity significantly increased in acute ATL in comparison to smoldering or chronic ATL. In families of ATL patients, no statistical difference in ADA activity between the anti-ATLA antibody-positive group and -negative group could be discerned. The enzyme activity in a patient with acute ATL, after a bone-marrow transplant, rapidly increased as leukemic cells increased in peripheral blood. These findings indicate that the levels of ADA activities in plasma from ATL patients reflect the condition of this disease. Thus, measurement of this enzyme activity offers a further parameter to distinguish subtypes of ATL, and is of prognostic and therapeutic value.
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PMID:Adenosine deaminase in plasma of patients with adult T-cell leukemia (ATL): correlation between enzyme activity and the ATL subtypes. 299 23

This report discusses a case of T cell chronic lymphocytic leukemia (T-CLL) in an elderly white man whose lymphocytes expressed a post-thymic phenotype except for the coexpression of T4 and T8 on 80% to 95% of the cells. Because of the uncommon phenotype, in vitro functional assays were performed that showed decreased mitogenic responses but normal helper activity for B cell immunoglobulin secretion and normal suppressor activity of lectin-induced mitogenesis. Morphologic evaluation by both light and electron microscopy and cytochemical staining were consistent with the "knobby" type T-CLL. Adenosine deaminase and terminal deoxynucleotidyl transferase (TdT) levels were low, but the acetylcholinesterase level was normal, which is consistent with the peripheral T cell phenotype. The patient underwent splenectomy, and the spleen cells showed very low levels of T3 and T4 by immunoperoxidase and undetectable levels by immunofluorescence. The morphology of the splenic infiltrate was not significantly different from that in the initial bone marrow. Human T cell leukemia virus (HTLV) antigen and antibody tests were negative. The cells in this leukemia apparently are derived from a transitional stage of maturation between the cortical and medullary thymocyte. A small subset of lymphocytes of identical phenotype to this leukemia has been identified in normal individuals.
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PMID:T cell chronic lymphocytic leukemia with lymphocytes of unusual immunologic phenotype and function. 387 Nov 60

Activity of terminal deoxynucleotidyl transferase (TdT), adenosine deaminase, and 5'nucleotidase and the cellular concentration of glucocorticoid (dexamethasone) receptor were determined in 25 patients with acute non-lymphocytic leukaemia. All patients were treated according to a common protocol. Increased activity of TdT (greater than 0.1 unit/microgram DNA) was found in 11 patients. This group of patients was shown to have higher remission and survival rates (p = 0.06) compared with patients with low activity of TdT. The glucocorticoid receptor concentration of the leukaemic blast cells ranged from 0 to 0.94 fmol/microgram DNA. Thirteen patients had blast cells with a glucocorticoid receptor concentration over 0.22 fmol/microgram DNA. These patients had significantly increased remission and survival rates (p = 0.006) compared with those with a low receptor concentration. This finding cannot be explained by a difference in sensitivity to glucocorticoids since these were not used as therapeutic agents. Adenosine deaminase and 5'nucleotidase activities both varied within two orders of magnitude. No correlation could be found between activities of these enzymes and remission or survival rate. These results show that measurements of TdT activity and the glucocorticoid receptor concentration yield valuable prognostic information in acute non-lymphocytic leukaemia.
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PMID:Glucocorticoid receptor concentrations and terminal transferase activity as indicators of prognosis in acute non-lymphocytic leukaemia. 626 1


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