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)

Cytogenetic studies indicate that most tumors are clonal (i.e. unicellular in origin) and have karyotypic alterations. These are not consistent, but non-random abnormalities are being increasingly identified by banding techniques, pointing to the sites on human chromosomes where genes important in neoplastic development are located. It is postulated that tumor progression occurs as a result of genetic lability within the neoplastic clone, leading to emergence of increasingly mutant subpopulations (often recognizable cytogenetically) with more malignant properties. In the context of this hypothesis, acute leukemia, chronic leukemia, and preleukemia can be viewed as differing only in the rate at which an abnormal hemic clone is expanding, with progression to a more aggressive phase (e.g. the "blast crisis" of chronic granulocytic leukemia) reflecting emergence of a new predominant subpopulation as the result of an additional genetic change. These concepts, and the cytogenetic data from which they have been derived, may help our understanding of basic tumor biology, and have some practical applications in the diagnosis of human neoplasms.
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PMID:Tumors as clonal proliferation. 10 6

Specific Activities of DNA-dependent RNA polymerases A and B have been determined in nuclei from leukocytes in acute and chronic leukemia. Enzyme activities, dependent on exogenous DNA template, were determined in homogenates of nuclei from isolated mononuclear cells or from isolated granulocytes. Activities of polymerases A and B have been found significantly elevated in homogenates of nuclei from mononuclear cells in acute myelocytic leukemia, while they were found subnormal in corresponding cell fractions from chronic myelocytic leukemia and chronic lymphatic leukemia. During cytostatic treatment polymerase activities were approaching normal values. The prognostic relevance of these data for the course of human leukemia is discussed.
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PMID:[DNA-dependent RNA polymerases in human leukocytes. II different specific activities of the polymerases A and B in acute and chronic leukemia and their prognostic relevance (author's transl)]. 105 88

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

Of 25 patients with chronic leukemia, there was clinical evidence of peripheral retinal microaneurysm formation in two of eight patients with chronic lymphocytic leukemia and six of 17 patients with chronic myelogenous leukemia. There was no proliferative retinopathy in any of the 25 patients. An elevated leukocyte count seemed necessary for microaneurysm formation in leukemia, although some patients with elevated counts had no microaneurysms. The prolonged leukocytosis of chronic leukemia can produce peripheral capillary dropout, vascular stagnation, microaneurysm formation, and, rarely, peripheral proliferative retinopathy similar to sickle cell disease.
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PMID:Peripheral retinal microaneurysms in chronic leukemia. 105 77

Occurrence of immune complexes in leukemia has been investigated by the 125I-Clq-binding test. A highly significant serum Clq-binding activity (Clq-BA) was demonstrated in 37% of patients with acute myelocytic leukemia, in 23% of patients with acute lymphocyte leukemia,and in 32% of those in blastic crisis of chronic myelocytic leukemia. Such a high Clq-BA is found only in 13% of cases with chronic leukemia. Incidence of increased serum Clq-BA is significantly higher during the blastic stage of leukemia than in complete remission. There is no correlation between the elevated Clq-BA and infections complicating acute leukemia, or with the chemotherapy given to the patients. The Clq-binding material exhibits properties similar to those of immune complexes.
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PMID:[Circulating immune complexes in human leukemias]. 107 Jan 56

Between 1985 and 1989, eight children underwent two successive bone marrow transplantations. The initial disease was chronic myelomonocytic leukemia in three patients, chronic myelocytic leukemia in two, acute M7 nonlymphoblastic leukemia in one, sickle cell anemia in one, and thalassemia major in one. The preparation in view of the second grafting included high-dose chemotherapy in all patients, associated with antithymocytic globulin transfusion and total nodal irradiation in three patients. Hematological recovery was similar after both graftings. Infectious complications were not more common following the second graft than after the first one. On the other hand, the rates of rejection and graft-versus-host disease were lower, probably due to a more intensive immunosuppressive therapy. The prognosis of chronic leukemia relapsing after a first graft does not seem to be improved by a second attempt.
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PMID:Second bone marrow transplantation in eight children. 146 68

Bleeding time, clot retraction, platelet factor 3 availability and platelet aggregation in response to ADP, epinephrine, collagen and ristocetin were studied in 12 cases of chronic leukemia which included eight of chronic myeloid leukemia, two of chronic lymphatic leukemia and two of CLL related disorders. One or more abnormalities in platelet function were detected in all the cases. Among the cases of CML, bleeding time was prolonged in one, clot retraction was impaired in one and PF3 availability was decreased in one case. Defects in platelet aggregation were variable. Among the cases of CLL and CLL related disorders, bleeding time was prolonged in two, clot retraction was impaired in one and PF3 availability was decreased in three cases. Platelet aggregation responses were significantly impaired in all the cases.
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PMID:Platelet function in chronic leukemias. 147 32

DNA from white blood cells from healthy controls demonstrates a restriction fragment length polymorphism (RFLP) of the Ha-ras oncogene locus after cleavage with the restriction enzymes BamH I or MspI plus HpaII, representing frequent and rare alleles. We have studied the RFLP of 15 patients with B-cell chronic lymphocytic (CLL) and of 16 patients with chronic myelogenous leukemia (CML). As in healthy controls the RFLP in the leukemic cells indicates the occurrence of frequent and rare Ha-ras alleles. But rare alleles are not more frequent in the patients than in the healthy control group. The frequency of rare Ha-ras alleles also does not differ between chronic lymphocytic and chronic myelogenous leukemia. While rare alleles of this oncogene locus occur in CML and CLL as frequently as in healthy controls, they do not reflect an inherent increased risk for chronic leukemia in man.
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PMID:Polymorphism of the human Ha-ras oncogene locus in chronic lymphocytic and chronic myelogenous leukemia. 168 29

Seventy five radiation-related leukemias (acute non-lymphocyte) in Hiroshima including 16 patients exposed to more than one Gray were cytogenetically examined. Statistical analysis of the data on the frequencies of chromosomal aberrations in survivors according to the bone marrow doses of DS86 estimation revealed that heavily exposed patients tended to have significantly higher aberration rates as compared with non-exposed patients. Furthermore, the chromosomal aberrations in the survivors were observed to be of a more complex nature and had characteristic findings of secondary leukemia. These observations therefore suggest that patients with a history of heavy exposure to atomic bomb radiation exhibit leukemic cells that originated from a stem cell which had been damaged by irradiation at the time of bombing and had been involved in the complex chromosome abnormalities. Molecular biological studies on transforming genes in acute and chronic leukemia and the bcr gene in chronic myelocytic leukemia have been performed in exposed and non-exposed groups. So far, no distinctive differences have been observed in the frequency and the sites of point mutations in N- and K-ras genes or in the rearrangement of the bcr gene, for a final conclusion of the specificity of radiation induced leukemia. Further retrospective studies require patient DNAs that developed in the early period of the atomic bomb exposure.
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PMID:Cytogenetic and molecular changes in leukemia found among atomic bomb survivors. 176 3

Eleven patients with chronic leukemia (7 with chronic lymphocytic leukemia and 4 with chronic myeloid leukemia) were evaluated with magnetic resonance (MR) imaging and T1 relaxation time measurements by use of a 1.5 tesla whole body MR scanner. Bone marrow biopsies were obtained from the posterior iliac crest (within 72 hours of the MR examination) in order to provide data on bone marrow cellularity and differential counts. The patients with chronic leukemia all showed a significant prolongation of the T1 relaxation times compared with the normal range for hemopoietic bone marrow.
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PMID:Prolonged T1 relaxation of the hemopoietic bone marrow in patients with chronic leukemia. 226 Dec 87


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