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)

Human B lymphocyte antigens analogous to the murine Ia determinants were found on myeloblasts and promyelocytes but not on more mature granulocytes. This was apparent by fluorescent staining with both human alloantisera and rabbit antisera to the isolated Ia-like proteins. The cells of patients with chronic myelocytic leukemia showed this difference especially clearly. Separation of the myeloblasts and promyelocytes by multistep density gradient fractionation produced a marked enrichment of the positive cells. The remaining cells from higher density fractions were more-mature neutrophils that were essentially negative. In acute myeloid leukemia, in which myeloid cells early in differentiation predominate, the vast majority of cells were strongly positive. Similar results were obtained with normal bone marrow cells. Here also, only the early forms of the myeloid series separated by gradient centrifugation had Ia antigens. Evidence was also obtained for the presence of Ia determinants on cells with the appearance of early erythroid precursors. Support for the presence of the Ia determinants on granulocyte-macrophage committed stem cells was provided by the inhibition of granulocyte colony formation in agar cultures following preincubation of normal bone marrow with antiserum and complement. Cross absorptions with purified preparations of immature cells provided evidence for the close similarity of the antigenic determinants on both myeloblasts and B cells. A 28,000-37,000-dalton bimolecular complex obtained from myeloblast membranes contained the Ia determinants and was similar to that obtained from peripheral blood B cell membranes.
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PMID:Expression of Ia-like antigen molecules on human granulocytes during early phases of differentiation. 7 38

Because all erythroid cells in chronic myelogenous leukemia are believed to arise from a common pluripotent stem cell, we studied the cellular distribution of fetal hemoglobin in patients with the disease to test whether cells with and without hemoglobin F have a common or separate pluripotent stem-cell origin. In a patient with chronic myelogenous leukemia and sickle/beta thalassemia, 17 per cent of the red cells during remission and 18 to 22 per cent during the blastic phase contained fetal hemoglobin. In 24 non-hemoglobinopathic leukemic patients 0.3 to 28 per cent of red cells contained hemoglobin F. Since the erythrocytes in chronic myelogenous leukemia are almost exclusively derived from the malignant clone, these data suggest that cells containing fetal hemoglobin originate from the same pluripotent stem-cell progenitor as those without hemoglobin F. The findings argue against a separate line of "partially switched" pluripotent stem cells as being responsible for maintenance of hemoglobin F production in the adult.
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PMID:Cellular distribution of hemoglobin F in a clonal hemopoietic stem-cell disorder. 27 Dec 71

A 10-year-old boy, who had been in an uninterrupted remission of acute lymphocytic leukemia (ALL) for six years, developed polycythemia vera (PV). One and a half months after detection of PV, he was found to have active leukemia. Both the polycythemia and leukemia receded with anti-leukemia therapy. Three possible explanations for the development of PV in a child with ALL are discussed: 1) PV was a part of his original ALL and recurred whtn patient relapsed. The PV phase was detected only during relapse because the patient was under close observation. 2) PV was a second neoplasm independent of ALL. 3) PV was part of a second leukemia which was different from the original leukemia; this new ALL was derived from a pluripotential cell line involving both erythroid and lymphoid elements. A precedent for this explanation has been observed in chronic myelogenous leukemia.
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PMID:Polycythemia vera in a child with acute lymphocytic leukemia. 28 32

The ability of cells derived from the K562 cell line to generate erythropoietic colonies was studied. The K562 cell line was derived from a patient with chronic myelogenous leukemia 8 yr ago by Lozzio and Lozzio. Rare benzidine-positive colonies formed when these cells were cloned in plasma clots (3 +/- 1/10(4) cells), and their number was not substantially increased by the addition of erythropoietin (9.5 +/- 1/10(4) cells). Sodium butyrate was capable of markedly enhancing the number of benzidine-positive colonies (19.5 +/- 1/10(4) cells) formed, while the combination of sodium butyrate plus erythropoietin exerted a synergistic effect on erythropoietic colony formation (57 +/- 4/10(4) cells). The K562 cell line is a long-term culture system that contains human erythropoietic stem cells. This cell line should be useful in future studies on the cellular and molecular events associated with human erythroid cell differentiation.
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PMID:Induction of erythropoietic colonies in a human chronic myelogenous leukemia cell line. 29 42

Peripheral blood and bone marrow specimens from 6 patients with Ph1-positive CML were evaluated for their content of erythropoietic and granulopoietic colony-forming progenitor cells. Specimens obtained from untreated patients showed marked increases in all compartments the most dramatic of which were for CFU-E and circulating CFU-C. This increased cell flow down the early stages of the red cell pathway in CML suggests that heightened proliferation and differentiation of primitive hemopoietic cells may be a more general phenomenon than previously suspected in this disease. In 5 of 6 patients, abnormal erythroid progenitors capable of proliferation and differentiation into hemoglobinized erythroblasts in cultures containing less than 0.002 units of erythropoietin/ml were regularly detected. In the 6th patient abnormal growth was not seen in cultures of the initial marrow obtained but was detected in cultures set up with peripheral blood taken 7 months later. The unexplained amplification of the erythropoietic compartment and the ability of some of these cells to mature in vitro in the virtual absence of erythropoietin is at variance with the anemia characteristic of untreated patients. This suggests the possibility of a major differentiation block at the level of CFU-E. Further studies of the properties of erythroid progenitors in these patients should help to provide new insights into the pathogenesis of CML and may provide useful markers for monitoring engrafted cell function after autotransplantation of patients in blast crisis.
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PMID:Abnormalities in the erythroid progenitor compartments in patients with chronic myelogenous leukemia (CML). 29 48

Proliferating populations of neutrophils, monocytes, eosinophils, erythroid cells, and T-lymphocytes from normal subjects or patients with various diseases can now be analysed by colony formation in semisolid cultures. These cultures accurately determine the number and proliferative activity of the precursor cells of each population and can also be used to monitor the levels of specific regulatory factors (for example, erythropoietin, colony-stimulating factor) in the serum or urine of such patients. Studies using semisolid cultures have shown that the leukemic cells in chronic and acute myeloid leukemia remain dependent on the normal regulator, granulocyte-macrophage colony-stimulating factor, for proliferation. The cultures have proved valuable in the prognostic assessment of acute leukemic patients and in monitoring impending changes in the clinical status of patients with acute or chronic myeloid leukemia or myeloproliferative disorders.
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PMID:In-vitro cloning techniques for hemopoietic cells: clinical applications. 33 9

The clinical and morphologic features of nine patients who initially presented with blastic leukemia and the Philadelphia chromosome were studied. Corresponding features were evaluated at the time of diagnosis of blast crisis in 19 patients who had a previous history of chronic myeloid leukemia (CML). Although many of the presenting symptoms and signs were similar, infections, lymphadenopathy, tissue infiltration and central nervous system involvement were more common in patients who presented with blastic leukemia. Marked leukocytosis, basophilia and marrow hypercellularity were present in both groups. Although patients in both groups had morphologic patterns that resembled acute leukemia, cytology suggestive of acute lymphocytic leukemia was more frequent in patients who initially presented with blastic leukemia. Megakaryocyte, platelet and erythroid abnormalities were more frequent in patients with a prior history of CML. Although there were clinical and morphologic features in the patients who presented with blastic leukemia which suggested the diagnosis of CML in blast crisis, chromosome studies were necessary to identify some of these patients. In both groups of patients multiple therapeutic regimens were used. Complete remissions were obtained in two patients; both presented with blastic leukemia, had "lymphoblastic" morphology and were treated with chemotherapeutic agents generally used for the treatment of acute lymphocytic leukemia. It appears that morphology of the blast crisis may be important in choosing the treatment regimen.
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PMID:Blast crisis as an initial or terminal manifestation of chronic myeloid leukemia. A study of 28 patients. 106 62

Irradiated mice reconstituted with bone marrow cells infected with a retrovirus carrying the bcr-abl oncogene of human chronic myeloid leukemia are subject to a range of neoplastic hematopoietic diseases, both myeloid and lymphoid. Comparison of DBA/2 and C57BL/6 mice has revealed a marked strain difference in susceptibility to the various tumor types. The present study, performed with BALB/c mice, indicates that the kinetics and nature of the induced disease can be modulated by the infection procedure, as well as the genetic background, and that retroviral regulatory sequences may influence the outcome. A distinctive clonal myeloproliferative disorder, somewhat akin to chronic myeloid leukemia but with prominent erythroid and mast cell components, as well as granulocytic excess, was characterized.
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PMID:Hematologic disease induced in BALB/c mice by a bcr-abl retrovirus is influenced by the infection conditions. 131 70

Erythropoietin-receptor (EpR) expression on bone marrow cells from normal individuals and from patients with chronic myeloid leukemia (CML) was examined by multiparameter flow cytometry after stepwise amplified immunostaining with biotin-labeled Ep, streptavidin-conjugated R-phycoerythrin, and biotinylated monoclonal anti-R-phycoerythrin. This approach allowed the detection of EpR-positive cells in all bone marrow samples studied. Most of the EpR-positive cells in normal bone marrow were found to be CD45-dull, CD34-negative, transferrin-receptor-positive and glycophorin-A-intermediate to -positive. This phenotype is characteristic of relatively mature erythroid precursors, ie, colony-forming units-erythroid and erythroblasts recognizable by classic staining procedures. Approximately 5% of normal EpR-positive cells displayed an intermediate expression of CD45, suggesting that these represented precursors of the CD45-dull EpR-positive cells. Some EpR-positive cells in chronic myeloid leukemia (CML) bone marrow had a phenotype similar to the major EpR-positive phenotype in normal bone marrow, ie, CD34-negative and CD45-dull. However, there was a disproportionate increase in the relative number of EpR-positive/CD45-intermediate cells in CML bone marrow. Even more striking differences between normal individuals and CML patients were observed when EpR-expression on CD34-positive marrow cells was analyzed. Very few EpR-positive cells were found in the CD34-positive fraction of normal bone marrow, whereas a significant fraction of the CD34-positive marrow cells from five of five CML patients expressed readily detectable EpR. These findings suggest that control of EpR expression is perturbed in the neoplastic clone of cells present in patients with CML. This may be related to the inadequate output of mature red blood cells typical of CML patients and may also be part of a more generalized perturbation in expression and/or functional integrity of other growth factor receptors on CML cells.
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PMID:Increased erythropoietin-receptor expression on CD34-positive bone marrow cells from patients with chronic myeloid leukemia. 137 Jun 38

The cytogenetic hallmark of chronic myelogenous leukemia (CML) is the Philadelphia chromosome (Ph1), which reflects a chromosomal translocation t(9;22) and a rearrangement of the ABL and bcr genes. This marker is found in all cells arising from the same malignant precursor cell and can be detected in CML cells of the myeloid, monocytic, erythroid, and B-lymphocyte lineage. It is, however, controversial as to whether T lymphocytes of CML patients carry this gene rearrangement. An answer to this question would clarify whether the translocation in CML occurs in a pluripotent hematopoietic stem cell or in a precursor cell already committed to certain lineages, but not the T-cell lineage. To address this question, we established T-cell clones from peripheral venous blood cells of four patients with CML and screened these clones for bcr-abl fusion transcripts by means of polymerase chain reaction and Southern blot analysis. In four T-cell clones of three of these patients, the bcr-abl transcript could be detected. None of 12 T-cell clones of the fourth patient disclosed detectable bcr-abl amplification product. Both CD4+ as well as CD8+ clones displayed fused bcr-abl sequences. These data imply that in CML some but not all T lymphocytes may originate from the Ph1-positive stem cell.
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PMID:Clonal analysis of bcr-abl rearrangement in T lymphocytes from patients with chronic myelogenous leukemia. 137 Oct 78


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