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)

Gangliosides from normal leukocytes and the cells of 25 patients with acute and chronic leukemia were tested for the presence of the disialoganglioside II3-alpha-N-acetylneuraminosyl-alpha 2----8-N-acetylneuraminosyllactosylceramide (GD3). GD3 was detected by immunostaining thin-layer chromatographs with an anti-GD3 monoclonal antibody (AbR24). Among the myeloid cells tested, acute leukemia cells were positive for GD3, whereas chronic leukemia cells and normal neutrophils did not have detectable GD3. A range of GD3 reactivity was apparent within the acute myeloid leukemia cells; gangliosides from pure myeloid leukemia cells stained more intensely than those from leukemia cells with monocytic characteristics. All lymphocytic leukemia cells (chronic and acute) contained GD3, but this ganglioside could not be detected in extracts from normal lymphocytes. A ganglioside extract from the cells of a patient with hairy cell leukemia was also positive for GD3 immunostaining. These results demonstrate that normal leukocytes and chronic myelogenous leukemia cells are distinguished from other lymphoid and nonlymphoid leukemia cells on the basis of GD3 ganglioside expression.
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PMID:Differential expression of ganglioside GD3 by human leukocytes and leukemia cells. 648 84

Acute febrile neutrophilic dermatosis, so called Sweet's Syndrome is a distinct dermatological disease defined by constant clinical and histological features: Eruption of painful, tender, raised erythematous plaques of face and neck with fever. Dense dermal infiltration with mature neutrophil polymorphs. Sweet's Syndrome may occur during the course of chronic or acute haematological diseases such as chronic myelogenous leukemia or acute non lymphoblastic leukemia. In all cases, the counts of Neutrophil Polymorphs were normal or above normal limits. We report a case of Sweet's Syndrome occurring during the aplastic period induced by the treatment of an acute myelo monocytic leukemia, and discuss the responsibility of white blood cells transfusion in genesis of typical histological aspect.
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PMID:[Lesions evoking Sweet's syndrome in acute leukemia: occurring during the stage of therapeutic aplasia]. 657 22

Various chemical inducers have effects on the induction of terminal differentiation of human myelogenous leukemia cell lines. We studied morphological and functional changes of human leukemia cells freshly obtained from patients using 12-0-tetradecanoyl phorbol-13-acetate (TPA), retinoic acid (RA) or dimethyl sulphoxide (DMSO). The myeloid leukemia cells cultured with TPA became adherent to plastic culture dishes, and then developed macrophage-like morphology with long filamentous pseudopods within 48 h incubation. They showed marked enhancement of the ability to phagocytose latex particles. But these acquired properties did not always parallel each other, suggesting that the mechanism of functional maturation of leukemic cells induced by chemical agents was not identical with that of morphological changes. On the other hand, the lymphoid leukemia cells did not show morphological and functional changes when cultured with the above inducers. It is suggested that exposure of leukemic cells to TPA for relatively short times (12-24 h) may be useful for determining whether they are of myeloid or lymphoid origin. These characteristic changes were also observed in leukemic cells from the myeloid or lymphoid crisis of chronic myelogenous leukemia.
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PMID:Differentiation of human leukemia cells and its usefulness for clinical diagnosis. 657 51

A 50-year-old man had chronic myelogenous leukemia and entered a blast crisis that was both morphologically and histochemically lymphoid. The blasts contained terminal deoxyribonucleotidyl transferase and expressed lymphoblastic leukemia-associated antigen. He rapidly entered remission with vincristine sulfate and prednisone therapy. Nevertheless, his blasts displayed a marker generally considered unique to myeloid cells: they selectively bound the granulocyte chemotaxin N-formyl-Met-Leu-Phe. In addition, some cells contained granules resembling those of basophils or mast cells. Such mixed myeloid-lymphoid features in chronic myelogenous leukemia blast cells may reflect malignant transformation of a stem cell capable of both myeloid and lymphoid differentiation, or they may reflect the dedifferentiation as a feature of malignant change.
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PMID:Chronic myelogenous leukemia. Development of blast crisis with both lymphoid and myeloid features. 658 Apr 70

Plasma levels of the circulating metabolite of prostaglandin (PG) E2, 15-keto-13,14-dihydro-PGE2 (KH2PGE2), were determined radioimmunologically after conversion to the stable degradation product 11-deoxy-15-keto-13,14-dihydro-11,16-cyclo-PGE2 (DKH2-cyclo-PGE2). In healthy volunteers a plasma level of 25 +/- 2 pg/ml (mean +/- S.E.M., n = 24) was found. The plasma level of KH2PGE2 was significantly decreased after administration of acetylsalicylic acid (4 x 1 g/24 hours). A significant elevation of the plasma levels of the circulating metabolite of PGE2 was observed in patients with bronchogenic carcinoma as compared to healthy controls, while no elevation was found in patients with chronic myeloid leukemia, lymphatic leukemia and non-Hodgkin lymphoma. The increased plasma levels of KH2PGE2 in the patients with bronchogenic carcinoma were independent of the clinical condition, histological type of tumor, tumor spread and therapeutic regimen. The results indicate that the elevated plasma level of the circulating PGE2 metabolite in patients with bronchogenic carcinoma is not an expression of malignant disease in general. On the other hand, the results do not suggest that the increase in the plasma level of KH2 PGE2 is a biochemical tumor marker closely related to a particular clinical feature of patients with bronchogenic carcinoma.
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PMID:Plasma levels of 15-keto-13,14-dihydro-prostaglandin E2 in patients with bronchogenic carcinoma. 658 45

A purified antigen from human acute myelogenous leukemia (AML) cells has been used to produce a myelogenous leukemia-associated monoclonal antibody. In limited FACS-IV analyses the monoclonal antibody to leukemia (CAMAL-1) as well as a conventional rabbit antiserum have been used to positively identify AML or chronic granulocytic leukemia patient cell samples. Neither CAMAL-1 nor the rabbit antiserum bound appreciably to acute lymphocytic leukemia cells, normal bone marrow, or normal peripheral blood leukocytes. CAMAL-1 was shown to be specific for AML cell extracts in the ELISA and was successfully used as an immunoadsorbent for the purification of the AML antigen from cell extracts. No significant levels of equivalent antigen were found when cell extracts from normal cells, lymphocytic leukemia cells, and lymphoma cells were similarly absorbed. These findings indicate that CAMAL-1 shows considerable specificity for an antigen associated with cells from patients with myelogenous leukemia.
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PMID:A monoclonal antibody to myelogenous leukemia: isolation and characterization. 658 67

A prospective study was done to assess the clinical utility of terminal deoxynucleotidyl transferase (TdT) and adenosine deaminase (ADA) assays in adult leukemia with a lymphoid phenotype. The study population consisted of 58 patients with adult lymphoblastic leukemia (ALL) at onset, 12 with lymphoblastic lymphoma, 15 with acute unclassifiable leukemia (AUL), and 30 with lymphoid or mixed acute phase of Philadelphia chromosome-positive (Ph' +) chronic myelogenous leukemia (CML). TdT was present in all cases of T-ALL, in 90% of non-T, non-B ALL, and absent in B-ALL; the ADA activity was significantly higher (P less than .01) in T-ALL. TdT was found in 75% of lymphoblastic lymphomas, in 78% of lymphoid, and in 50% of mixed CML transformations; higher ADA activity correlated with TdT positivity in AUL and CML blastic transformations (P less than .001). TdT-positive ALL had a better chance of response to therapy than TdT-negative ALL (P less than 0.01), but survival was not statistically different. TdT was undetectable in the peripheral blood of patients with ALL in complete remission and within the normal range in bone marrow (0.1%-8% of nucleated cells); median ADA activity was as in control subjects. Relapsing ALL patients had TdT and ADA enzymatic activities as before therapy; TdT immunofluorescence test (IF) was positive in 69% of bone marrow and in 100% of CNS relapses. Twenty percent of TdT-positive ALL at onset became TdT-negative in bone marrow at relapse. TdT IF test was instrumental in detecting meningeal leukemia but neither TdT nor ADA could be used as indicators of complete remission or impending relapse because TdT-positive cells were present in normal marrows and wide fluctuations of TdT IF values and of ADA activity were observed in remission.
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PMID:Clinical utility of terminal deoxynucleotidyl transferase and adenosine deaminase determinations in adult leukemia with a lymphoid phenotype. 658 63

Twenty-five cases of Ph1-positive acute leukemia (AL) are described, 13 presenting an acute lymphocytic leukemia (ALL) and 12 an acute non-lymphocytic leukemia (ANLL). In 12 cases coarse, pink, peroxidase-negative cytoplasmic granules were found in the leukemic cells. These granules have not been described in Ph1-negative AL and their presence appears to be pathognomonic of Ph1-positive acute leukemia. The leukemias of three patients consisted of both lymphoid and myeloid clones while the cells of two patients had lymphoid and myeloid markers simultaneously present in the same cells. Cytogenetic studies were useful for monitoring response and some patients clearly acquired a Ph1-negative status during clinical remission. The disease appears to be more resistant to chemotherapy than Ph1-negative acute leukemia. While similar to chronic myelocytic leukemia (CML) in the Ph1 translocation, Ph1 AL differed from it both in age at presentation and response to therapy.
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PMID:Ph1-positive acute leukemia. 659 42

Blood and/or bone marrow cells from patients with hematological malignancies, chronic lymphocytic leukemia (CLL), chronic myeloid leukemia in blastic phase, acute lymphoid leukemia, acute myeloid leukemia, prolymphocytic leukemia, multiple myeloma and myelofibrosis, were incubated with Lonidamine at different concentrations (50, 100 and 160 micrograms/ml) for 1-2 h. B lymphocytes of CLL had the highest sensitivity to the drug: a decrease of more than 30% in the viable nucleated cells was recorded in 8 out of 10 experiments. Subsequent in vivo studies were performed to investigate the effectiveness of Lonidamine in the treatment of CLL. The drug was administered orally for a period of 7 days to 19 selected patients, both previously treated and untreated, in different stages of the disease. Only 5 patients responded: 2 of them had a significant decrease (greater than 30%) in the lymphocyte count, and the remaining 3 showed an appreciable reduction of the spleen (1 case) and of the lymph node size (2 cases). Generalized myalgia was the most common side effect induced by Lonidamine.
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PMID:Lonidamine in the treatment of chronic lymphoid leukemia. 671 3

Bone marrow transplantation offers two potential therapeutic advantages over more conventional therapy of leukemia. It allows more intensive treatment to be given without regard to marrow toxicity and allows in the case of allogeneic marrow an additional immunotherapeutic effect through graft-versus-host disease (GVHD). Initially, allogeneic transplants in HLA matched sibling donors were only employed in end-stage patients. Although there were encouraging results in terms of long-term therapeutic effects, the overall mortality was prohibitive. Subsequently, patients were transplanted in remission with a marked improvement in overall survival in both acute lymphocytic leukemia and acute non-lymphocytic leukemia. The major obstacles to further improvement in the therapeutic effects of this procedure have been identified (i.e., GVHD, viral infection, and relapse in ALL) and are subject to intensive investigations that already show encouraging results. Syngeneic marrow transplantation is limited for obvious reasons, but early results have shown significant therapeutic effects, in particular, in chronic myelogenous leukemia. These results have encouraged others to use autologous bone marrow. Marrow contamination with unseen tumor cells is being approached by pharmacologic and immunologic techniques designed to "purge" marrow of tumor cells. Animal and initial clinical studies have been encouraging.
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PMID:Bone marrow transplantation: current results in leukemia. 676 16


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