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)

A mouse monoclonal antibody (MA-10) was raised using cells of a patient with AML (M2). MA-10 reacted with leukemic cells in 44 out of 60 AML cases. Intense reaction was observed especially in 32/38 cases with M1 and M2, as well as 9/9 with common ALL and 2/2 with T-ALL. No appreciable reaction was observed with mature blood cells with only exception of T cells. In-vitro addition of MA-10 did not affect the growth of GM-CFC and BFU-e from two patients with CML in chronic phase. MA-10 identified three polypeptides of approximate mol. wt of 74,000, 50,000 and 30,000.
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PMID:A monoclonal antibody with reaction spectrum covering acute leukemia and T-lineage cells. 325 78

We used a complement-dependent cytotoxic assay to study the expression of DR antigens by hemopoietic progenitor cells derived from normal marrow and from the blood of patients with chronic phase chronic myeloid leukemia (CML). Almost all normal and CML day-12 granulocyte-macrophage colony-forming cells (d12 GM-CFC) and erythroid burst-forming units (BFU-E) expressed DR antigens. A primitive progenitor cell, the "blast colony-forming cell" (Bl-CFC), also expressed DR antigens whether derived from normal marrow or CML blood. The expression of DR antigen by normal and CML Bl-CFC was similar but the density of DR antigens on CML d12 GM-CFC and BFU-E was much greater than that of their counterparts from normal marrow. The similarity in DR antigen density on normal and CML Bl-CFC means that purging of CML marrow using a DR-specific antibody would not select in favor of normal cells and thus would not be useful in an autograft setting.
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PMID:Increased DR antigen expression by committed hemopoietic progenitor cells but not primitive progenitor cells in chronic myeloid leukemia. 342 91

Myeloid cytoreduction leading to hematologic remissions is frequently seen among patients with chronic phase Philadelphia-positive chronic myelogenous leukemia (CML Ph') treated with leukocyte interferon (IFN-alpha). In order extend our understanding of the events associated with interferon-induced myeloid cytoreductions, we have examined the changes in granulocyte-monocyte colony-forming cells (GM-CFC) in such CML Ph' patients. A total of 28 CML Ph' patients in hematologic remissions following IFN-alpha treatment had a median GM-CFC of 12 (range, 0-182)/1 X 10(5) bone marrow cells. This was significantly lower than the median GM-CFC of 104 (range, 44-815; p less than 0.01) in 22 untreated or minimally treated CML Ph' patients and the median of 72 (range, 30-204; p less than 0.05) in 18 normal controls. A gradual decline in the GM-CFC numbers from a median of 105 to a median of 1.8 was seen in six responding patients who were studied serially over a median period of 7.5 months. In these patients, we also observed a profound decline in the number of aspirated bone marrow nucleated cells and a decline in the bone marrow cellularity. The effect of treatment interruption for a median of 13 days was studied in five patients. In three of the patients who had received IFN-alpha for less than or equal to 6 months, treatment interruption resulted in rapid increase in the GM-CFC, while the GM-CFC did not change in the remaining two patients, who received IFN-alpha for one and two years. We conclude that treatment of CML patients with IFN-alpha resulted in a progressive decline of the bone marrow GM-CFC. The initially expanded pool of committed myeloid stem cells declines gradually, and at the time of hematologic remission the number of GM-CFC/10(5) nucleated bone marrow cells is lower than that of normal controls. In the early phases of IFN-alpha treatment, this inhibitory effect is rapidly reversible, but it seems to persist when the treatment is extended over more than one year.
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PMID:Changes in granulocyte-monocyte colony-forming cells among leukocyte-interferon-treated chronic myelogenous leukemia patients. 346 Aug 11

We measured the number of blast colony-forming cells (Bl-CFC) in the blood of 11 patients with untreated chronic granulocytic leukemia (CGL). The culture system used detects three types of Bl-CFC (Types I, II and III) in normal marrow, of which Bl-CFC (I) are the most primitive and might represent the putative hemopoietic stem cell. The mean numbers of Bl-CFC (I) in CGL blood, normal bone marrow and normal blood were 134 +/- 29 (+/- SEM), 127 +/- 21 and 1.5 +/- 0 respectively per 1 X 10(6) mononuclear cells. These findings are consistent with the concept that CGL is due to a primary increase in stem cell numbers with secondary increases in committed progenitor and leukocyte numbers.
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PMID:Primitive progenitor cells in the blood of patients with chronic granulocytic leukemia. 346 57

Bone marrow (BM) cells from 15 patients with chronic granulocytic leukemia (CGL) and 12 normal donors were placed in liquid culture for 4-7 days in the presence of fetal calf serum (FCS) or human AB serum. BM cells were plated in agar for GM-CFC growth at day 0, day 4, day 7 of culture, in the presence of human placenta conditioned medium (HPCM). The recovery of GM-CFCs on day 4 in FCS was 86 +/- 18 and 15 +/- 18% from normal or CGL BM cells respectively (p = 0.005). The recovery of GM-CFCs on day 4 in human AB serum was comparable for normal (66 +/- 48%) and CGL (69 +/- 32%) BM cells. Similar results were obtained on day 7 of culture. Cytochemical staining of agar plates showed a sharp drop of macrophage colonies in CGL BM cells kept in FCS cultures on day 4-7, when compared to both normal BM cells and baseline colonies. These data suggest that the survival in liquid culture of GM-CFCs from patients with CGL is dependent on a factor present in human and not in fetal calf serum. This is not the case for normal GM-CFCs.
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PMID:Human serum-dependent survival of GM-CFCs in vitro from patients with chronic granulocytic leukemia. 346 15

Inhibitory activity in extract from human blood granulocytes was tested on granulocyte-macrophage colony formation in vitro. The inhibition depended on the type of serum used. With mouse BMC and FCS in the cultures, extract corresponding to 2.5 X 10(4) granulocytes/ml reduced the colony number by 35%, and extract from 2 X 10(5) cells caused maximal inhibition (80-90%). With HS and mouse BMC the colony number was reduced by only 11-12%, but stronger inhibition (55%) was observed when the serum concentration was reduced. With both types of sera the total cell number per culture plate was reduced relatively more than the colony number. Human GM-CFC were as sensitive as mouse GM-CFC, and extract from CML granulocytes inhibited less (p less than 0.01) than extract from normal cells. Biochemical studies indicated that the inhibitor is a protein with a molecular weight of 30-60,000. Lactoferrin, a putative inhibitor of CSF production, did not inhibit spontaneous or CSF-induced colony formation in these studies.
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PMID:Colony inhibiting factor in mature granulocytes from normal individuals and patients with chronic myeloid leukemia. 347 14

Anti-MY9 is an IgG2b murine monoclonal antibody selected for reactivity with immature normal human myeloid cells. The MY9 antigen is expressed by blasts, promyelocytes and myelocytes in the bone marrow, and by monocytes in the peripheral blood. Erythrocytes, lymphocytes and platelets are MY9 negative. All myeloid colony-forming cells (CFU-GM), a fraction of erythroid burst-forming cells (BFU-E) and multipotent progenitors (CFU-GEMM) are MY9 positive. This antigen is further expressed by the leukemic cells of a majority of patients with AML and myeloid CML-BC. Leukemic stem cells (leukemic colony-forming cells, L-CFC) from most patients tested were also MY9 positive. In contrast, MY9 was not detected on lymphocytic leukemias. Anti-MY9 may be a valuable reagent for the purification of hematopoietic colony-forming cells and for the diagnosis of myeloid-lineage leukemias.
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PMID:A monoclonal antibody reactive with normal and leukemic human myeloid progenitor cells. 659 Sep 30

Prostaglandins of the E series (PGE) have varying effects in vitro on normal granulocyte/macrophage (CFU-GM) progenitors. When added directly to cultures, PGE inhibits growth of normal 7 and 14 day bone marrow CFU-GM in a dose-dependent manner, while CML CFU-GM are refractory to PGE inhibition. The plant diterpene forskalin, a potent activator of intracellular cyclic AMP, inhibited normal and CML CFU-GM, indicating that the response of CML cells to increased intracellular cyclic AMP is normal. Low dose forskalin, which potentiates activators of adenyl cyclase, showed additive effects with PGE on normal CFU-GM cells, however, showed no additive effects of PGE and forskalin, suggesting that PGE failed to activate adenyl cyclase. Normal CFU-GM incubated with PGE for two hours showed a significant increase in CFU-GM growth, and removal of adherent cells prior to exposure to PGE abrogated this effect. CML cells did not respond to a 2-h exposure to PGE, and removal of adherent cells from these cultures had no effect. Normal and CML CFU-GM showed dose-dependent increases in proliferation in the presence of PGF2. These studies confirm that CML CFC-GM are refractory to inhibition by PGE, and show that these cells respond normally to increased levels of intracellular cyclic AMP. Response of CML cells to PGF2 alpha is normal, and conversion of PGE to PGF could result in increased granulocyte progenitor proliferation.
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PMID:Further studies on mechanisms of abnormal prostaglandin response by chronic myelogenous leukaemia granulocyte/macrophage progenitors. 659 11

Marrow culture studies revealed a spectrum of qualitative and quantitative defects in granulocyte-macrophage progenitors (GM-CFC) of patients with chronic myeloid leukemia in chronic phase and blastic crisis. Parallel culture studies and terminal transferase determinations revealed that a significant proportion of patients in blastic crisis possess two coexisting acute phase clones, one lymphoblastic and one myeloblastic. Measurement of response to and production of T cell growth factor showed that the leukemic blast cells from patients with TdT-positive blastic crisis produced the factor, but did not exhibit a proliferative response to exogenous factor. This phenotype was identical to that observed in TdT-positive acute lymphoblastic leukemia. Additional regulatory defects were identified in CML, since leukemic GM-CFC proliferation was resistant to inhibition by concentrations of prostaglandin E, which are markedly inhibitory for normal GM-CFC. The self-renewal or recloning capacity of GM-CFC was also identified as a unique feature of some patients with CML. The addition of retinoic acid to primary cultures of leukemic GM-CFC completely abolished this recloning capacity.
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PMID:Phenotypic evaluation of chronic myeloid leukemia. 694 81

In order to study the pathogenesis of juvenile-type chronic myelocytic leukemia (CML), we examined the colony-forming capacity and colony composition in the bone marrow (BM) and peripheral blood (PB) of three children with juvenile-type CML. Large numbers of granulocytes and macrophage colonies were formed by BM and PB cells. Whole agar culture staining revealed that especially macrophage colonies increased in comparison with normal controls. After removal of carbonyl iron-laden cells with a magnet or deprivation of cells adherent to glass from BM cells, the number of macrophage colonies markedly reduced in comparison with the number of colonies formed by untreated BM cells, suggesting that some of the macrophage colony-forming cells (M-CFC) may have phagocytic and/or adherent activity. Radiation sensitivity and thymidine suicide rate of these M-CFC were not different from those of granulocyte colony-forming cells (G-CFC). The predominance of M-CFC in juvenile-type CML may be one of the reflections of fetal-type myelopoiesis since M-CFC are predominant in cord blood and PB in the neonatal period. Moreover, considerable numbers of erythroid-colony-forming units (CFU-E) were present in PB of all patients. It may be concluded that juvenile-type CML is a panmyelopathy with the predominance of M-CFC.
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PMID:Characterization of hemopoietic precursor cells in juvenile-type chronic myelocytic leukemia. 695 Nov 3


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