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)

Twenty-seven consecutive patients with previously untreated, or minimally treated benign phase Philadelphia-chromosome-positive, chronic myelogenous leukaemia (CML) were treated with partially purified human leucocyte (alpha) interferon; 24 of the 27 patients responded to therapy achieving either haematological remission (20 patients) or partial haematological remission (four patients). In the responding patients the peripheral white blood cells declined from a median of 89.6 X 10 X 10(9)/l to 4.5 X 10 X 10(9)/l. The serum lactate dehydrogenase declined from a mean of 8.36 Katal/l (492 mu/ml) to 2.8 Katal/l (165 mu/ml), and the vitamin B12 levels declined from 1492 pg/ml to 838 pg/ml. Fifteen patients had splenomegaly. The spleen size normalized in four and decreased by a median of 30% in 10 additional patients. The bone marrow cellularity fell from a median of 100% to a median of 62%. In seven of the 24 responding patients, followed for greater than or equal to 6 months, the percentage of Ph1-positive cells in the bone marrow declined to a median of 70% (range 5-75%). Alpha interferon was found to be an effective therapeutic agent for controlling the myeloid proliferation in CML, and in partially restoring the nonclonal haematopoietic cells in some of the patients.
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PMID:Chronic myelogenous leukaemia: haematological remissions with alpha interferon. 346 63

The mononuclear peripheral blood cells from eight patients with chronic myelocytic leukaemia (CML) were incubated in cell suspension culture in the presence of the phorbolester 12-O-tetradecanoylphorbol 13-acetate (TPA). TPA caused the treated cells to adhere and to acquire morphological and functional features characteristic of macrophage-like cells. Using isoelectric focusing distinct changes in the isoenzyme profiles of carboxylic esterase, acid phosphatase, hexosaminidase and lactate dehydrogenase were detected in the TPA-exposed cells. Besides an increase in the number and staining intensity of isoenzymes of all enzymes, TPA triggered the new expression of a monocyte-specific esterase isoenzyme isoenzyme and of the tartrate-resistant acid phosphatase isoenzyme. The latter two isoenzymes represent further parameters of the monocyte/macrophage complex. The results indicate that immature leukaemic cells arrested along the granulocytic cell axis retain the ability to transform to macrophages.
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PMID:Induction of differentiation in chronic myelocytic leukaemia cells by the phorbolester TPA. 346 54

Back pain due to vertebral changes as early feature of acute lymphocytic leukemia (ALL) in childhood has been infrequently reported. There are 8 previously described patients with similar clinical and laboratory data, suggesting a biologically unique subset of ALL. Characteristic findings of this rare primary manifestation of leukemia are lack of significant organomegaly or lymphadenopathy, normal or low white blood cell count with predominance of lymphocytes and rarely circulating lymphoblasts, normal platelet count, uric acid and lactate dehydrogenase values. In the following report we make a further attempt to confirm the hypothesis of a subset of ALL, demonstrating two additional patients with characteristic features of ALL presenting with vertebral changes and low leukemic burden.
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PMID:[Changes in the vertebrae as an initial symptom of leukemia]. 347 11

Fresh leukaemia cells from the peripheral blood of 6 patients with B-chronic lymphocytic leukaemia (CLL) were cultured in the continuous presence of the phorbolester 12-O-tetradecanoylphorbol 13-acetate (TPA) for in vitro induction of differentiation. Upon treatment with TPA the cells showed distinct morphological changes consisting of cytoplasmic and nuclear enlargement, vacuolisation and protrusion of cytoplasm, eccentric location of nuclei with perinuclear clear zones, and oval to elongated cell forms. Isoenzyme profiles of the enzymes carboxylic esterase, acid phosphatase, hexosaminidase and lactate dehydrogenase (LDH) were analysed by isoelectric focusing on polyacrylamide gels. An increase in the number and in the staining intensity of isoenzymes were observed for all 4 enzymes in the TPA-exposed cells indicating a maturation along the B cell pathway. TPA triggered the new expression of the tartrate-resistant acid phosphatase isoenzyme, a marker of hairy cell leukaemia (HCL) cells, and of the hexosaminidase I isoenzyme, a marker of multiple myeloma cells. The induced phenotypic changes are suggestive of differentiation to stages corresponding to those of HCL cells or 'pre-plasma cells'.
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PMID:Morphological and isoenzymatic differentiation of B-chronic lymphocytic leukaemia cells induced by phorbolester. 348 41

The ability of 12-O-tetradecanoylphorbol 13-acetate (TPA) to induce stable phenotypic changes that serve as markers of differentiation was examined in the non-T/non-B leukemia cell lines KM-3 and REH and in the pre-B leukemia cell lines BV-173 and NALM-6. Isoenzymes of the enzymes carboxylic esterase, acid phosphatase, hexosaminidase, and lactate dehydrogenase (LDH), separated by isoelectric focusing on horizontal polyacrylamide thin-layer gels, were used to monitor induced changes. TPA in different concentrations completely or partially inhibited cell proliferation, but had no drug-related cytotoxicity. No increase in the number of nitro-blue-tetrazolium-reducing cells nor adherence to plastic surface was found. In all four cell lines, TPA caused an increase in number and staining intensity of esterase, acid phosphatase, and LDH isoenzymes. The resulting isoenzyme profiles corresponded to those seen at more mature intermediate stages of B-cell proliferation, but did not indicate a terminal differentiation to mature B cells. The loss of the hexosaminidase I isoenzyme, which is a marker of immature hematopoietic cells, was a further indicator of induced maturation. These results demonstrate that while TPA is capable of inducing various immature non-T/non-B and pre-B cell lines to differentiate, the differentiation progression appears to be restricted to intermediate stages, in contrast to the terminal differentiation inducible in myeloid cells.
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PMID:Pre-B and non-T/non-B leukemia cell lines BV-173, KM-3, NALM-6, and REH: changes in isoenzyme profiles during induction of differentiation. 348 15

Biochemical analysis has been used to monitor the induction of differentiation in cultured human T-leukemia cell lines (CCRF-CEM, HPB-ALL, JM and MOLT-4) by the phorbolester 12-0-tetradecanoylphorbol 13-acetate (TPA). The isoenzymes of carboxylic esterase, acid phosphatase, hexosaminidase and lactate dehydrogenase were separated by isoelectric focusing on horizontal thin-layer polyacrylamide gels and stained by histo-cytochemical methods. TPA inhibited the proliferative activity in all four cell lines and led to aggregation of cells seen as floating clusters. TPA induced an increase in number and staining intensity of isoenzymes of all four enzymes in the cell lines studied. This corresponds to an induced isoenzymatic maturation as the progressive increase in number and staining intensity of the isoenzymes parallels the differentiation along the T-cell pathway. However, regardless of the initial stage of arrested differentiation, the cell lines could be induced only to differentiate to a certain more mature stage, but could not be triggered to differentiate terminally with regard to expression of isoenzyme patterns.
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PMID:T-leukemia cell lines CCRF-CEM, HPB-ALL, JM and MOLT-4: changes in isoenzyme profiles during induction of differentiation. 349 47

Serum ferritin concentrations were determined in 142 untreated cases of acute leukaemia. No correlation between type of leukaemia as defined by morphology and immunology and the level of serum ferritin was found. Samples were also tested for lactate dehydrogenase (LDH), phosphohexose isomerase (PHI), B-glucuronidase (B-gluc), leucine aminopeptidase (LAP), and C-reactive protein (CRP) levels. Serum ferritin was significantly correlated with serum PHI, LAP, and LDH concentrations but not with leukaemic mass as assessed by total white blood cell count (WBC). Ferritin and CRP levels were also significantly correlated suggesting that ferritin may behave to some extent like an acute phase reactant in acute leukaemia.
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PMID:Serum enzyme and ferritin concentrations in acute leukaemia. 350 81

To identify adults with acute nonlymphocytic leukemia at risk for the development of central nervous system involvement, we performed periodic cerebrospinal fluid examinations on patients in remission. Among 58 consecutive patients monitored during first remission, central nervous system leukemia developed in nine (16 percent). Four patients, including one who was symptomatic, had central nervous system leukemia detected simultaneously with marrow relapse. Five additional patients were asymptomatic and continue to have bone marrow remission. Following central nervous system and systemic treatment, two of these five patients have never had relapse, and three had relapse in the bone marrow five, 10, and 21 months later. Factors at diagnosis associated with the subsequent development of central nervous system leukemia were elevated leukocyte count, serum lysozyme and lactate dehydrogenase, extramedullary infiltration including splenomegaly, and monocytic (FAB M4 or M5a) morphology. In six of 17 patients (35 percent) with monocytic morphology, central nervous system leukemia developed compared with only three of 41 patients (7 percent) with other subtypes (p = 0.02). Discriminant analysis identified leukocyte count, splenomegaly, and M4 or M5a morphology as the most important risk factors and led to a mathematical formula that correctly identified 90 percent of the patients. Although the risk of central nervous system leukemia in adults with acute nonlymphocytic leukemia is too low to justify routine prophylaxis, those patients recognized to be at a greater risk should receive prophylaxis or be monitored closely with periodic lumbar punctures.
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PMID:Central nervous system involvement in acute nonlymphocytic leukemia. A prospective study of adults in remission. 366 83

Cellular and humoral markers of malignancy play several roles at many levels in the evaluation and staging of children with cancer. Cytogenetic analysis of constitutional cells can be used to determine the genetic risk of developing certain cancers, such as retinoblastoma and Wilms' tumor in high-risk families. Urinary metabolites of neuroblastoma have been studied not only for accurate diagnostic ability in children with "small round cell" tumors, but as a screen for the presence of the tumor in large normal populations. Markers are valuable as prognostic factors at the time of cancer diagnosis; for example, the use of cell surface antigens and cytogenetics in leukemia phenotyping, leading to alterations in initial therapy. Once found at diagnosis, both specific and nonspecific markers can then be utilized to follow the regression and recurrence of a malignancy, such as serum ferritin in neuroblastoma or lactate dehydrogenase in non-Hodgkin's lymphoma. Presence of cell surface antigens to which monoclonal antibodies can be directed are becoming increasingly helpful in both tumor localization, such as in radioisotope scanning, and in therapeutic intervention, such as in purging autologous bone marrow of malignant cells prior to use as a rescue after massive cytoreduction. Finally, cellular markers have lead to a better understanding of the basic biology of particular neoplasms; for example, gene rearrangements in lymphoma, which will ultimately lead to better diagnostic and therapeutic ability.
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PMID:The use and significance of biologic markers in the evaluation and staging of a child with cancer. 371 38

Serum total lactic dehydrogenase (LDH) levels have been found to be significantly higher in 21 children with acute lymphoblastic leukaemia (ALL) at initial diagnosis than the values of 12 children who achieved remission. The mean value of serum LDH levels in patients with high-risk factors was 2347 +/- 1490 U/ml (range 430-5460 U/ml), while in patients at standard risk it was 652 +/- 385 U/ml (range 110-1320 U/ml). The serum LDH values were above 1320 U/ml in 70% of the 13 children with high-risk factors. The serum isoenzyme patterns were analyzed in 17 of these children at the initial diagnosis. Although LDH-3 and LDH-2 were prominent at the time of diagnosis; LDH-2 and LDH-1 were the predominant isoenzymes in remission. The highest concentrations of LDH-3 were observed in the high-risk group at diagnosis and the ratio of LDH-3 to LDH-2 exceeding 1.0 was found in children who had high-risk factors, but not in any patients in the standard risk group.
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PMID:Prognostic value of the determination of serum lactic dehydrogenase and its isoenzymes in children with acute lymphoblastic leukaemia. 385 4


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