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)

Rabbit antisera have been produced to an acute myelomonocytic leukaemia (AMML)-derived cell line (RC2a) and a histiocytic lymphoma derived cell line (U937) having macrophage characteristics. The antisera were screened by complement-mediated cytotoxicity and immunofluorescence (cytofluorograph analysis) against separated leukaemic (122 patients plus 13 cell lines) and normal haematologic cell populations (60 preparations from 20 donors plus 10 B-lymphoblastoid cell lines). The sera were absorbed with pooled B-lymphoblastoid cell lines including the autologous B-lymphoblastoid cell line to RC2a (CESS-B) or alternatively with B-CLL and T-CLL cells. All leukaemic cell populations were confirmed using the markers SIg, E-rosette receptor, cALL antigen, alpha-naphthyl butyrate esterase and myeloperoxidase. Rabbit anti-RC2a (Adherent cells) (RARC2a(Ad) ) and rabbit anti-U937 (RAU937) recognised antigens common to immature myeloid monocyte and T-lymphocyte lineage but did not react by cytotoxicity, absorption or cytofluorographic analysis with cells of B-lymphocyte lineage (B-lymphoblastoid or B-CLL) and reacted only occasionally with cALL patients' cells (includes pre B phenotype). These sera reacted with peripheral blood monocytes but not with other mature blood leucocytes. RAU937 reacted with a major mononuclear population from normal marrow and with more differentiated myeloid leukaemia cells. RARC2a(Ad) and RAU937 detected overlapping subgroups of myeloid leukaemia (AMoL, AMML, AML and CML) patients and Null-ALL and T-ALL patients. These subgroups are now being examined for prognostic significance.
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PMID:Rabbit antisera to cell lines RC2a and U937: antigens expressed on human leukaemic cells of myeloid, monocyte and T-lymphocyte lineage. 681 43

The cellular origin of the K 562 cell line, established from a patient in the blast crisis of chronic myeloid leukemia has been investigated. In agreement with previous reports, an erythroid differentiation was observed. A minority of immature, but hemoglobinized erythroblasts were identified both by electron microscopy and by immunofluorescence using an antibody to gamma-globin chains. Embryonic and fetal hemoglobin (Hb) were synthesized. Hemin increased the number of erythroblasts as well as the absolute amount of Hb synthesized: the Hb pattern was also significantly modified. By cytochemical ultrastructural detection of peroxidase activity (PA), a weak PA, distinct from granulocytic peroxidases, was found exclusively in the nuclear envelope and rough endoplasmic reticulum in a small number proportion of cells. In its localization this PA resembled that of normal and leukemic promegakaryoblasts. The addition of sodium butyrate or dimethylformamide markedly increased the number of these cells (up to 30%) but did not modify their cytoplasmic maturation. No modification of Hb synthesis was observed. Cloning of the K 562 line revealed a marked heterogeneity from one clone to another in Hb production, in the phenotype of Hb synthesis, and in the inducibility by butyrate or dimethylformamide. An inverse relationship between the number of cells with PA and Hb production was found in the different clones. Recloning some of these primary clones resulted in secondary clones, which displayed properties similar to those from which they had originated. All attempts to obtain granulocytic differentiation by addition of different inducers failed. These results clearly indicate that the K 562 cell line arises from the proliferation of bipotent stem cells, these cells possessing variable capacities of differentiation toward erythroid and presumably megakaryocytic cell lineages.
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PMID:Heterogeneity in the cellular commitment of a human leukemic cell line: K 562. 694 84

Results of chromosome studies of blood and bone marrow cells from 101 patients with Ph1 positive chronic myeloid leukemia (CML) confirm the assumptions that clinical and morphologic manifestations of the disease correlate with karyotype peculiarities of leukemia cells. Several variants of the clinical course of CML may be distinguished. One is the variant with a short chronic phase and a comparatively long terminal phase. In blastic crisis the blast cells are peroxidase negative and do not possess cytoplasmic inclusions. Acute transformation occurs without any additional chromosome damage. The second, more common form is less severe because of longer chronic phase but it has a short and grave acute stage. The blast cells present definite signs of myeloid differentiation, they have basophilic or neutrophilic cytoplasmic granules and are peroxidase positive. Marker i(17q) often combined with trisomy 8 is a characteristic chromosome abnormality in the terminal stage of this variant. The third type has an extremely long chronic phase but ends in a rapidly progressing severe and resistant to therapy "lymphoid" blastic crisis. Blast cells have typical "lymphoid" morphology, they are peroxidase negative and contain granular PAS positive substance. Various additional chromosome changes appear in the terminal stage. Future studies of a larger series of patients may possibly reveal more CML variants.
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PMID:Correlations between the clinical course, characteristics of blast cells, and karyotype patterns in chronic myeloid leukemia. 694 65

A Ph1 chromosome positive chronic myeloid leukemia patient whose chronic phase lasted 7.5 years experienced a blastic transformation originating in the spleen. The spleen was infiltrated with undifferentiated blast cells that on cytogenetic analysis had a hyperdiploid karyotype and were Ph1 chromosome positive. The blast cells were negative for PAS, peroxidase. Sudan black and esterase stains. They were non-T, non-B with TdT activity. Remission was achieved in response to prednisone, vincristine, and adriamycin. Ph1 positive cells were present with cells responding to PHA stimulation throughout the course of the disease. A Giemsa-11 staining procedure male possible the ascertainment of a No. 9 translocation chromosome in blastic crisis cells that had also been present in Ph1 chromosome positive cells early in the disease. The presence of this translocation initially in myeloid cells and subsequently in apparent lymphoid cell types suggests the origin of this patient's leukemia as a pluripotential stem cell.
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PMID:9;22;15 complex translocation in Ph1 chromosome positive CML revealed by Giemsa-11 procedure in apparent lymphoid cells of blastic crisis. 694 32

The behaviour of phagocytosis and that of PGE1 and PGE2 in the circulating granulocytes of normal and leukaemic subjects was investigated by the comparison of latex particles and the PAP (peroxidase-antiperoxidase) immuno-enzymatic method respectively. Generally speaking, it was found that chronic myeloid leukaemia and acute myeloblastic leukaemia were accompanied by a marked reduction in phagocyting capacity, whereas this is apparently normal in CLL and ALL. PCE values, on the other hand, were well down in lymphatic leukaemia, AML and AMML, but not in CML, where high PGE (especially PGE2) was noted both basally and after phagocytosis. That the PGE take part in phagocytosis is shown by their redistribution in phagocyting cells, with elective accumulation in the membrane and around the engulfed material.
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PMID:[Behavior of PGE1 and PGE2 in the granulocytes of normal and leukemic subjects during phagocytosis in vitro]. 695 84

White blood cells from 22 patients with leukemia and lymphoma were studied for the presence of terminal deoxynucleotidyl transferase with a peroxidase-antiperoxidase method. The enzyme was detected in leukemic cells of 5 patients with acute lymphoblastic leukemia and 1 patient with chronic myelogenous leukemia, whereas 16 patients with different forms of leukemia or lymphoma were negative for this enzyme. Comparative studies using a biochemical and an indirect immunofluorescence assay revealed complete concordance between these three methods.
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PMID:Histochemical demonstration of terminal deoxynucleotidyl transferase in leukemia. 702 72

Four cases of acute nonlymphocytic leukemia with primitive basophilic differentiation are presented. In all four cases, study revealed Philadelphia chromosome negativity, and in none were there clinical findings of chronic granulocytic leukemia. In each case, the leukemic blasts contained granules that failed to stain for peroxidase content but stained positively with toluidine blue. The former result could have led to the misclassification of the cases as lymphoid leukemias. Three of the four patients had physical findings that may have been due to circulating histamine excess. The histochemical and clinical features of these cases suggest that certain examples of leukemia with basophilic differentiation represent a distinctive variant of acute nonlymphocytic leukemia.
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PMID:Acute nonlymphocytic leukemia with basophilic differentiation. 708 45

We established a novel T cell line, designated TK-6, from a patient with T cell lineage blast crisis of chronic myelogenous leukemia (CML) complicated by hypercalcemia. A surface marker study showed T cell phenotype, cluster designation (CD)4, CD5 and CD7. Light and electron microscopic examination revealed myeloperoxidase (MPO)-negative, however, ultrastructural examination under certain specific conditions demonstrated that some cells were MPO-positive. The TK-6 cell karyotype carried a t(9;22)(q34;q11) and additional chromosome aberrations, including a deletion of the long arm of chromosome 6 and the abnormality of chromosome 7. Southern blot analysis showed rearrangement of the T cell receptor beta-chain (TCR beta) gene and the major breakpoint cluster region (bcr) gene. Northern blot analysis detected the expression of the parathyroid hormone-related protein (PTHrP) gene, however, the proviral genome of human T cell leukemia virus type I (HTLV-I) was negative. This cell line will provide a valuable resource for the analysis of the relationship between T cell lineage crisis and myeloid differentiation and for the analysis of humoral hypercalcemia of malignancy (HHM) or leukemia.
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PMID:Establishment and characterization of a novel cell line, TK-6, derived from T cell blast crisis of chronic myelogenous leukemia, with the secretion of parathyroid hormone-related protein. 747 85

A 56-year-old woman was admitted with pyrexia, cough, and dyspnea on August 21, 1991. Physical examination revealed anemia in the palpebral conjunctivas and moist rales at the right lower lung field. Neither the Liver nor spleen was enlarged. Examination of the peripheral blood showed a hemoglobin level of 8.1 g/dl, a platelet count of 14.8 x 10(4)/microliters, and a white blood cell count of 2,800/microliters, with 7% blasts and 8% megakaryocytes. Tear drop-like erythrocytes, agranular neutrophils, and erythroblasts were also seen in the peripheral blood. Examination of the bone marrow showed 15% peroxidase positive blasts, and many micromegakaryocytes. Cytogenetic studies for bone marrow cells revealed the existence of the Philadelphia (Ph1) chromosome. Bone marrow biopsy showed normal cellularity with increase of megakaryocytes and advanced myelofibrosis. Breakpoint cluster region (bcr) rearrangement analysis using the peripheral blood mononuclear cells revealed M-bcr rearrangement. According to the Hannover classification for myeloproliferative disease, she was diagnosed as having CML with advanced myelofibrosis followed by CML with megakaryocytic increase. Since she had neutrocytopenia and severe infectious disease, she received a subcutaneous injection of 125 micrograms of G-CSF. Not only increase of the white blood cell count, but also disappearance of blasts, improvement of anemia, increase of the platelet count, and improvement of myelofibrosis were observed.
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PMID:[Hematologic abnormalities in a patient with chronic myelogenous leukemia with advanced myelofibrosis were improved by G-CSF]. 751 Nov 82

Clinical studies have indicated that the posterior cingulate cortex is intimately involved in verbal and auditory memory. The present study was performed to obtain anatomical evidence for the above proposal. The connections of the auditory cortical areas with the posterior cingulate cortex in the macaque monkey were examined by retrograde and anterograde tracing methods using wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP). WGA-HRP was injected into either area TA, TB or TC in the superior temporal auditory cortex. Area TA was reciprocally connected with the posterior cingulate cortex, whereas areas TC and TB were not. The rostral two-thirds of area TA had major connections with the caudomedial lobule in the retrosplenial cortex (CML of Goldman-Rakic et al., 1984) and a minor one with area 23b. The caudal third of area tA was connected only with area 23b. However, neither labeled cells nor terminals were observed in areas 23a, 23c, 29, 30 or 31 in the posterior cingulate cortex following a WGA-HRP injection into the caudal, intermediate or rostral portion of area TA. The present finding suggests that verbal and auditory memory impairment in patients with damage to the posterior cingulate cortex is largely due to damage to the CML and area 23b and not to the other posterior cingulate areas.
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PMID:Neural connections of auditory association cortex with the posterior cingulate cortex in the monkey. 756 98


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