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)

4 cases of chronic monocytic leukemia were observed during several years. In 2 patients there was a final appearance of blastic crisis. During the course of the disease the activity of the naphthylacetate-esterase in the monocytes increased, but the PAS-reaction was lowered. By the help of two cases for comparison - one patient suffering from a chronic myeloid leukemia and intermediate monocytic phase, the other one from a panmyelopathia and monocytic reaction - the morphological resemblance of these phenomena is demonstrated, which cytochemically cannot be separated.
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PMID:[Cytochemical data in chronic monocytic leukemia]. 5 1

The diseases discussed in this paper include chronic lymphocytic leukemia, monocytic leukemia, chronic granulocytic leukemia, acute leukemias, Hodgkin's disease, and lymphosarcoma. Cutaneous manifestations of these disorders are often sufficiently different to indicate a certain leukemia or lymphoma. The cutaneous manifestations of leukemias and lymphomas may help the clinician suspect the diagnosis.
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PMID:Skin manifestations of leukemias and lymphomas. 27 26

The various leukemias in Hokkaido for the past 20 years are analysed in its change of the mortality rate, the type of leukemia, and the clinical picture. The observation years are divided into 4 periods: I (1951-1957), II (1958-1962), III (1963-1967), IV (1968-1972). 1. The adjusted mortality rate of leukemia shows a rising tendency through these periods: I (1.7), II (3.0), III (3.5), IV (3.6). 2. The adjusted age-specific mortality rate of leukemia in period II, III, and IV, show a remarkable increase in all age brackets compared with period I, especially in older age brackets. The rate of the "60-69 years old" bracket gradually rises as I (3.1), II (4.8), III (5.9), IV (7.2). The rate of the "over 70 years old" bracket is I (1.3), II (1.8), III (5.0), IV (9.3). It is characteristic that these brackets has the highest mortality rate in period IV. 3. Some comparisons between period I and IV are described as follows: (1). Monocytic leukemia had decreased from 10.6% (I) to 1.4% (IV) and chronic myelogenous leukemia has slightly increased in period IV. (2). In acute type, the cases of aleukemic leukemia tends to increase in period IV and its initial symptoms changes into mild gradually. (3). In chronic type in period IV, splenomagaly is common in the initial symptom and while blood cell counts in these cases are above 10 x 10(4)/cmm.
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PMID:[Chronological changes in leukemias in Hokkaido (author's transl)]. 98 94

Foam cells in the spleen, bone marrow, liver and lymph nodes were examined on the 73 reliably recorded and sampled leukemia autopsy cases encountered at Kobe University from 1958 to 1972. Although the substances stored in the foam cells were biochemically unknown, the foam cells in leukemia could be morphologically classified into two types: The one was identified with the Gaucher type, but the other was not identified with the sea-blue type and might be considered as to be the transitional type described in another report. Foam cells could be found in the spleen of 6 out of 12 cases of chronic myeloid leukemia, one out of 2 cases of chronic lymphatic leukemia, one out of 7 cases of leukemic lymphosarcoma, one out of 9 cases of acute lymphatic leukemia, and none in 3 cases of monocytic leukemia. In acute myeloid leukemia, the incidence of foam cells in the spleen was 47.5% in 40 cases, and acquired lipidoses were more frequently seen in cases under 19 years of age, in male cases, in cases with an enlarged spleen over 400 g, and in cases of over 4 months' duration.
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PMID:Secondary lipidosis in leukemia. 99 40

Peripheral blood from a child with adult-type (Philadelphia chromosome positive) chronic granulocytic leukemia was found to contain large numbers of cells capable of colony formation in tissue culture. The majority of the colonies contained granulocytic cells. The source of these granulocytic colonies was found in a population of myeloblasts, promyelocytes, and myelocytes which could be separated from the more mature granulocytic cells of the peripheral blood by sedimentation of the buffy coat on Ficoll-Hypaque. The predominance of granulocytic colonies is in contrast to our observations previously made on the peripheral blood of children with "juvenile" type(Ph1 chromosome negative)CGL in which large numbers of exclusively monocytic colonies were produced in tissue culture. These current studies, when interpreted in light of relevant clinical data, suggest that the "juvenile" and "adult" types of CGL represent two very different forms of chronic leukemia in childhood. The Ph1 chromosome negative form may be classified as a monocytic leukemia with a granulocytic component but the Ph1 chromosome positive adult form, even when it occurs in a child, appears to be a true granulocytic leukemia.
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PMID:In vitro colony-forming characteristics of chronic granulocytic leukemia in childhood. 105 30

The juvenile type of "chronic myelogenous" leukemia (CMLJT) is a rare disease with only 40 cases reported to date. Clearly distinguishable from adult CML on both clinical and laboratory grounds, is is often confused with "congenital" leukemia, pseudoleukemia, leukemoid reactions or chronic granulomatous disease. According to studies of muramidasuria and colony-forming cells it is neither a chronic nor a granulocytic leukemia. It is a panmyelopathy with monocyte predominance and should thus be classified as a variant of myelo-monocytic leukemia. We review reported responses to chemotherapy and splenectomy and report our results with cytosine arabinoside in the treatment of 2 cases with this disease. Chemotherapy may prolong life and splenectomy may be useful in some cases; but the survival rate is 0%, justifying new approaches.
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PMID:"Chronic myelogenous" leukemia of juvenile type. Report of two cases and review of therapy. 106 53

Pharmacologic differentiation of the promyelocytic leukemia HL60 is associated with an increase in cellular tyrosine phosphatase activity. We asked (a) if this increase might, at least in part, be due to changes in a transmembranous protein-tyrosine phosphatase, CD45; and (b) if CD45 changes similarly in other differentiating leukemias. Differentiation of HL60, several chronic myelogenous leukemias, a monocytic leukemia (THP-1), and a monoblastoid leukemia (U-937) could be induced by phorbol ester, 1,25-dihydroxy vitamin D3, dimethyl sulfoxide, or cyclic AMP analogues. This differentiation was associated with a marked increase in (a) total cellular tyrosine phosphatase activity (2-4-fold as measured by the ability to dephosphorylate a tyrosine-phosphorylated peptide); (b) CD45-specific tyrosine phosphatase activity (2-4-fold); (c) CD45 cell surface expression by flow cytometry (2-5-fold); (d) synthesis of both exon B-dependent M(r) 205,000 and exon ABC- M(r) 185,000 CD45 proteins, as revealed by immunoprecipitation with antisera specific for CD45 isoforms. Both isoforms have enhanced electrophoretic mobility when isolated from the differentiated cells. This enhanced mobility did not appear to be due to decreased stoichiometry of CD45 phosphorylation on serine/threonine residues. Interestingly, 12-O-tetradecanoylphorbol-13-acetate transiently reduced CD45 protein-tyrosine phosphatase activity in the chronic myelogenous leukemia cell RWLeu4 without altering the CD45 amount (as measured by cell surface immunofluorescence). Modulation of CD45 tyrosine phosphatase activity (and protein levels) may play a role in differentiation or in maintaining cells in a nonproliferative state or may represent a phenotypic marker of differentiation.
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PMID:Differentiation-induced changes in protein-tyrosine phosphatase activity and commensurate expression of CD45 in human leukemia cell lines. 153 52

The levels of leukocyte alkaline phosphatase (LAP) messenger RNA (mRNA) are evaluated in B and T lymphocytes, monocytes, and polymorphonuclear cells (PMNs), and this transcript is found to be present only in PMNs. Precursors of the myelomonocytic pathway, represented by leukemic cells isolated from several cases of chronic myelogenous leukemia (CML) in its stable and blastic phase and acute myelogenous leukemia (AML), are devoid of LAP transcript. These data support the notion that LAP is a marker of the granulocyte terminal differentiation. Despite the absence of LAP mRNA in both the myeloid and the lymphoid precursors, nuclear run-on experiments show constitutive transcription of the LAP gene in leukemic cells obtained from AML, CML, as well as acute lymphoblastic leukemia (ALL) and B-cell chronic lymphocytic leukemia (B-CLL). In CML and in chronic myelo-monocytic leukemia (CMML) PMNs, granulocyte colony-stimulating factor (G-CSF) specifically accumulates LAP mRNA without showing a substantial increase in the rate of transcription of the LAP gene. Once increased by G-CSF, LAP mRNA is very stable, showing a half-life of more than 4 hours in the presence of actinomycin-D. G-CSF is suggested to play a pivotal role in the modulation of LAP transcript in PMNs.
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PMID:Expression of leukocyte alkaline phosphatase gene in normal and leukemic cells: regulation of the transcript by granulocyte colony-stimulating factor. 170 29

Microangiopathic haemolytic anaemia was diagnosed in the course of haematopoietic and lymphatic disorders such as chronic granulocytic leukemia, chronic myelofibrosis, chronic lymphatic leukemia, Osler's disease, chronic monocytic leukemia, and lymphoplasmocytic lymphoma, in 11 patients (6 women and 5 men) aged between 33 and 81 years (mean age 58.8 years) treated at the Haematological Out-Patient Clinic of the Postgraduate Medical Education Centre within 1977-1987. The following laboratory tests were carried out: 1) morphology of the peripheral blood and bone marrow, especially some haematological parameters concerning erythrocytes and blood platelets; 2) biochemical tests reflecting erythrocytes disintegration; 3) haemostasis. All examined patients suffered from haemolytic anaemia of various degree with characteristic changes in erythrocyte shape (helmets, tear-drops etc.). Haemolytic origin of anaemia was confirmed by the increased LDH activity. In the majority of patients no compensative stimulation of haematopoiesis (reticulocytosis, red blood cells hyperproliferation in bone marrow) was seen. Clinical symptoms of haemostatic disorders such as haemorrhagic diathesis and vein thrombosis were diagnosed in 50% of the patients. Blood platelet counts ranged from markedly decreased to significantly increased. Bone marrow smears did not show increased number of megacariocytes. Bleeding time was prolonged in the majority of examined patients while prothrombin index--decreased). Abnormal fibrinogen levels (decreased or increased) were found in the majority of patients with fibrin degradation products. Microangiopathic haemolytic anaemia in these patients differ from the typical Moschowitz's disease clinically probably due to the lack of compensative stimulation of erythropoiesis and lower thrombocytopenia.
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PMID:[Microangiopathic hemolytic anemia in patients with diseases of the hematopoietic and lymphatic systems]. 262 5

By in situ hybridization on chromosome, phytohemagglutinin (PHA)-stimulated lymphocytes obtained from normal individuals showed slight polymorphism in terms of distribution of rDNA among Nucleolar Organizer Region (NOR) chromosomes probably due to racial differences, although their interindividual distinct polymorphism had been reported in the U.S.A. Three chronic and one acute myelogenous leukemias (CML and AML) and one chronic monocytic leukemia (CMoL) were also analysed for the distribution of rDNA among NORs. The distribution patterns in leukemia cells were found to be significantly different from those in the cells of normal individuals. Although genetic alteration of normal leukocytes was not disregarded, the changes of rDNA distribution in leukemia cells are demonstrated in this study. The Ph1 chromosome in CML carried a greater amount of rDNA. The rDNA distribution in Ph1-negative cells obtained from patients showed almost the same pattern as that of Ph1-positive cells. In AML, the t(8;21) carried a smaller amount of rDNA. Trisomic chromosome 21 in CMoL carried extra rDNA copies on its NOR. Based on these data, leukemia cells seem to show variability of rDNA distribution especially on marker chromosomes, contrary to the non-polymorphic patterns of normal lymphocytes. Thus a strong relationship between marker formation and abnormal distribution of rDNA could be suggested.
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PMID:Ribosomal RNA gene (rDNA) distribution in human leukemia cells by in situ hybridization on chromosome. 279 60


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