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)

Two cases of childhood myelodysplastic syndrome with chromosome abnormalities involving band 11p15 are described. The first case, with inv(11)(p15q23), had a complex clinical course; the initial diagnosis was aplastic anemia, then refractory anemia with excess of blasts in transformation (RAEB-t), and finally, before death, chronic myelomonocytic leukemia with hematologic features similar to those of chronic myelogenous leukemia (CML). The second case, with t(4;11)(p13;p15), progressed from RAEB to acute myelogenous leukemia (M2). In the literature, we found 12 patients with nonlymphocytic leukemia and chromosome abnormalities involving band 11p15, including seven cases with t(7;11)(p13-p15;p15); four cases (including the present case 1) showed CML-like hematologic features. It is suggested that translocations involving 11p15 are a nonrandom chromosome abnormality in nonlymphocytic leukemia.
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PMID:Childhood myelodysplastic syndromes with 11p15 translocation. 329 71

Chronic myeloid leukaemia (CML) includes five subtypes, and the term should be used in the same way as the term chronic lymphoid leukaemia to refer to a group of related conditions. The subtypes of CML are: 1. Chronic granulocytic leukaemia (CGL) (95% of all CML; 90% are Ph+, BCR+, 5% are Ph-, BCR+); 2. Juvenile CML (extremely rare; Ph-, BCR- in the few so far examined); 3. Chronic neutrophilic leukaemia (CNL) (extremely rare; Ph-, BCR- in the few so far examined); 4. Chronic myelomonocytic leukaemia (CMML). CMML with low or normal leukocyte counts is classified as a myelodysplastic syndrome; CMML with high leukocyte count is both myelodysplastic and myeloproliferative. Ph-, BCR-; 5. Atypical CML (aCML). Intermediate between CGL and CMML but has distinctive features. Ph-, mostly BCR-. Significance of few reported BCR+ uncertain. Markedly worse survival than CGL and probably worse than CMML. Definition needs refining. Types 2, 3, 4 and 5 account for 5% of all CML. CGL, CMML, aCML and CNL can be diagnosed in the great majority of cases from the morphological profile of presentation peripheral blood films, but high-quality Romanowsky staining is essential.
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PMID:Haematological classification of the chronic myeloid leukaemias. 333 55

The antigenic phenotype of myelomonocytic progenitors [colony-forming unit granulocyte-macrophage (CFU-GM)] from 33 patients with chronic myeloproliferative disorders was investigated using four cytotoxic monoclonal antibodies. Monoclonal antibodies S3-13, S8-6, and S16-144 which recognize normal hemopoietic progenitors of different lineages reacted with almost all CFU-GM. R1B-19 monoclonal antibody identified two subpopulations of myelomonocytic progenitors (type 1 and 2 CFU-GM), as reported previously in normal subjects. In 3 of 11 patients with chronic myelogenous leukemia, in 1 of 2 patients with chronic myelomonocytic leukemia, and in 2 of 4 patients with polycythemia vera, a higher proportion of the more immature CFU-GM (type 1) was detected in bone marrow cells. The more differentiated CFU-GM (type 2) is not detectable in normal peripheral blood. By contrast, in 14 of 15 chronic myelogenous leukemia patients, in 1 of 2 chronic myelomonocytic leukemia patients and in 3 of 8 patients with idiopathic myelofibrosis, it was present in high to very high proportions. It is clear from these findings that the antigens present on normal CFU-GM are expressed in chronic myeloproliferative disorders. The proportion and distribution of type 1 and 2 CFU-GM, on the other hand, are very different from those observed in the normal subjects.
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PMID:Antigenic phenotype of myelomonocytic progenitors (CFU-GM) in chronic myeloproliferative disorders. 345 79

Clinical, hematologic, and prognostic differences between Philadelphia chromosome (Ph1)-positive and Ph1-negative chronic granulocytic leukemia (CGL) have been described. However, Ph1-negative disease may be a mixture of other entities. The authors identified 24 patients given the diagnosis of Ph1-negative CGL after evaluation by the Hematology Department of the Mayo Clinic between January 1976 and August 1984. Each patient was Ph1-negative, and a bone marrow examination was interpreted as CGL. Initial peripheral blood and bone marrow samples were available for review in 22 patients. Their disorders were reclassified as chronic myelomonocytic leukemia (13 patients), chronic myelomonocytic leukemia in transformation (1 patient), preleukemic syndrome (3 patients), and undifferentiated chronic myeloproliferative disease (5 patients). Median survival for the 22 patients was 17 months.
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PMID:Ph1-negative chronic granulocytic leukemia: a nonentity. 345 94

Cellular oncogenes have been localized at the breakpoints of characteristic chromosomal rearrangements occurring in certain hematologic malignancies. This has been reported to result in aberrant expression of the involved oncogenes. Over 90% of chronic myelogenous leukemia (CML) is characterized by a reciprocal translocation that brings c-abl from chromosome 9 to chromosome 22, and c-sis from chromosome 22 to chromosome 9. To investigate the possible role of these two oncogenes in the leukemic process, we studied their expression in a number of fresh samples obtained from patients with various forms of leukemia, by Northern blot analysis using c-onc probes. Seven of 24 samples obtained from patients with either CML or chronic myelomonocytic leukemia expressed a normal 4.0-kilobase (kb) c-sis transcript. C-sis expression was found only in the accelerated/blast phases but not in the chronic phase of CML. All of the CML Philadelphia chromosome-positive (Ph1+) samples expressed an aberrant 8-kb c-abl transcript. The expression of c-sis in
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PMID:C-sis and C-abl expression in chronic myelogenous leukemia and other hematologic malignancies. 345 50

The reactivity of a murine IgG1 monoclonal antibody, NHL-30.5, that detects a surface antigen expressed on acute myeloid leukemia (AML) cells has been studied. Initially raised against the HL-60 cell line, NHL-30.5 has subsequently reacted with blood and/or bone marrow cells from 15 of 19 AML patients studied at presentation or in relapse, 1 patient with chronic myelomonocytic leukemia (CMML), 1 patient with myelofibrosis (MF) who subsequently developed AML, and 1 of 5 patients with acute lymphoblastic leukemia (ALL). It has shown no detectable binding to cells from AML patients in remission (0/3), patients with chronic myelogenous leukemia in chronic phase (CML) (0/7), normal bone marrow (0/9), normal peripheral blood mononuclear cells, granulocytes, platelets, erythrocytes, monocytes, or splenocytes by radioimmunoassay or fluorescence analysis using flow cytometry. HL-60 cells induced to differentiate following incubation in the presence of dimethylsulfoxide (DMSO) lost their ability to bind NHL-30.5. Immunoprecipitation of iodinated HL-60 cell surface components showed the antigen to have an apparent mol./wt of 180,000 under reducing conditions. These results suggest that the antigen is different from any other myeloid antigens reported to date, and may be useful in further studies of leukemic cell phenotypes.
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PMID:NHL-30.5: a monoclonal antibody reactive with an acute myeloid leukemia (AML)-associated antigen. 385 4

An unusual myelodysplastic syndrome with similar features in two patients is described. The entity is characterized by a maturation arrest at the myelocyte stage, strikingly clumpy chromatin, and a clinical course marked primarily by difficulties caused by anemia and thrombocytopenia. Electron microscopic description of the characteristic abnormal clumpy chromatin cells is included. While the disorder is unquestionably a myelodysplastic syndrome, it is clearly distinct from chronic myelogenous leukemia, chronic myelomonocytic leukemia, and the spectrum of refractory anemias with excess blasts.
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PMID:A variant myelodysplastic syndrome with multilineage Pelgeroid chromatin. 394 1

A technique for dual staining of cells using terminal deoxynucleotidyl transferase (TdT) and myeloperoxidase (MPO) is described. The technique has been applied to cells of two patients. One patient had chronic myelomonocytic leukemia evolving into acute myelomonocytic leukemia. The other patient had chronic myelogenous leukemia in blast crisis. Our findings indicate that TdT and MPO are exclusive markers except for a rare precursor cell with dual staining in one patient. This study supports the concept of acute mixed leukemia.
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PMID:Simultaneous evaluation for terminal deoxynucleotidyl transferase and myeloperoxidase in leukemia. 628 39

A four-year-old child with recurrent infections and increasing hepatosplenomegaly over a three-year period was evaluated. Increased numbers of myeloid precursors packed the bone marrow and infiltrated the peripheral blood. A diagnosis of chronic myelogenous leukemia (CML) was considered but could not be confirmed by laboratory studies appropriate for the types of CML usually observed in childhood. Examination of the patient's peripheral blood smears revealed many atypical monocytoid cells with unipolar hairy projections. Scanning electron microscopy showed these to be leukemic monoblasts with characteristic broad-based ruffles on the cell surface. A population of myeloid precursors possessing narrow ridge-like profiles was also observed. Progressive infiltration of the spleen caused hypersplenism which necessitated splenectomy. Subsequently, massive liver and bone marrow involvement led to the patient's death. Terminally, the proliferating blast cells were demonstrated to be leukemic monoblasts by analysis of cytochemical staining patterns, surface immunoglobulins, serum lysozyme levels, and monocyte-mediated antibody-dependent cellular cytotoxicity studies. The findings in this case are most compatible with a diagnosis of chronic myelomonocytic leukemia (CMML), a condition not previously described in childhood. Several myeloproliferative disorders with prolonged survival have been reported in children, but special studies were not performed to determine which cell lines were abnormally proliferating. The similarities between these children and our patient with CMML suggest that monocyte studies may be useful in the diagnosis of these unusual disorders, provide insights into their pathogenesis, and aid in the selection of appropriate therapy.
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PMID:Chronic myelomonocytic leukemia in childhood. 694 Apr 41

We developed a sensitive method of measurement of granulocyte colony-stimulating factor (G-CSF) by an enzyme-linked immunosorbent assay, which we applied in the plasma of the bone marrow aspirate in 70 patients with various hematological disorders. The lowest limit of detection by this method is 2 pg/ml. G-CSF was detected in all but two of the patients. Compared to the G-CSF level in normal healthy controls, those in non-Hodgkin's malignant lymphoma, aplastic anemia, agranulocytosis and multiple myeloma were significantly higher, while the level in refractory anemia was not different. The G-CSF level in acute myelogenous leukemia patients was either elevated or decreased regardless of the French-American-British subgroup. The level in acute lymphoblastic leukemia was not different from the normal value, as was that in refractory anemia with an excess of blasts, and that in chronic lymphocytic leukemia. A patient with chronic myelomonocytic leukemia showed initial elevation of G-CSF with normalization after entering complete remission. The G-CSF level in chronic myelogenous leukemia was significantly decreased, although one patient in hematological remission who was under alpha-interferon therapy showed normal levels. The level in polycythemia vera was not significantly different from the normal value. The G-CSF level for the entire group showed an inverse, although not statistically significant, correlation with the percentages of myeloid cells of the bone marrow (r = -0.174, p = 0.1703, n = 80). These results are thought to reflect the regulatory mechanism of granulopoiesis in the bone marrow in various hematological disorders, and it is concluded that this method may be of clinical use in the treatment of patients with these disorders and in the selection of candidates likely to benefit from G-CSF administration.
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PMID:The levels of granulocyte colony-stimulating factor in the plasma of the bone marrow aspirate in various hematological disorders. 872 2


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