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 megakaryoblastic cell line, designated MEG-01, was established from the bone marrow of a patient with blast crisis of Philadelphia (Ph1) chromosome-positive chronic myelogenous leukemia. MEG-01 cells grew in single-cell suspension with a doubling time of 36 to 48 hours. Under the usual culture conditions, approximately half of the cells adhered to the culture flask with extention of pseudopods. MEG-01 cells were positive for the periodic acid-Schiff reaction, alpha-naphthyl acetate esterase, and acid phosphatase, and negative for myeloperoxidase, alpha-naphthyl butyrate esterase, naphthol AS-D chloroacetate esterase, and alkaline phosphatase. Ultrastructural platelet peroxidase was positive in MEG-01 cells. Cytoplasmic factor VIII (FVIII)-related antigen was weakly positive in larger MEG-01 cells by both an indirect immunofluorescent technique with monoclonal antibodies and a direct immunoperoxidase technique using horseradish peroxidase-conjugated conventional rabbit anti-human FVIII antibody. Platelet glycoprotein (GP) IIb/IIIa antigen was uniformly demonstrated on the surface of MEG-01 cells by both indirect immunofluorescent and immunoperoxidase techniques using antiplatelet GP IIb/IIIa monoclonal antibodies; platelet GP lb antigen was demonstrated only in the cytoplasm of larger MEG-01 cells. MEG-01 cells possessed no markers for B or T lymphocytes or for myeloid cells. Chromosome analysis of this cell line revealed a human male hyperdiploid karyotype with a modal chromosome number of 56 to 58. The Ph1 chromosome was observed in all karyotypes analyzed. This novel human megakaryoblastic cell line may provide a useful model for the study of human megakaryopoiesis and of the biosynthetic mechanisms of proteins unique to megakaryocytic lineage.
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PMID:Establishment of a novel human megakaryoblastic leukemia cell line, MEG-01, with positive Philadelphia chromosome. 299 11

An attempt was made, by treatment with 12-O-tetradecanoyl-phorbol-13-acetate (TPA), to induce differentiation in Ph1-positive (PB-1049) and Ph1-negative (LN-1049) B lymphoblastoid cell lines established from a patient with chronic myelogenous leukemia, and a Ph1-positive line (PB-1049-T) derived from a tumor nodule formed by inoculation of PB-1049 cells into nude mice. The changes induced by TPA in all lines were consistent with differentiation towards plasma cells, and included enhanced clustering of floating cells, reduced DNA synthesis, increase of the cytoplasm/nucleus ratio and appearance of a large amount of rough endoplasmic reticulum in the cytoplasm. Immunoglobulin concentration was estimated by ELISA in the supernatant of the three cell lines. Remarkable increases were observed in PB-1049 and PB-1049-T cultures treated with TPA. These results suggest that the Ph1-positive as well as Ph1-negative B lymphoblastoid cell lines examined have the potential to perform the proper functions of B lymphocytes in vitro.
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PMID:Differentiation by a tumor promoter of lymphoblastoid cell lines with and without Ph1 chromosome from a chronic myelogenous leukemia patient. 311 62

Mature polymorphonuclear neutrophilic leukocytes (PMNL) from a 2.5-year-old female with infantile chronic myelogenous leukemia (CML) were stimulated with phorbol myristate acetate or opsonized zymosan. The resulting enzymatic NADPH oxidation and the cellular O2- release and luminol-enhanced chemiluminescence were measured. The patient's PMNL responded normally in all respects. Thus, mature infantile CML PMNL undergo a normal respiratory burst following either soluble or particulate stimulation. Our review of the literature emphasizes the importance of studying a well-defined population of PMNL in patients with myelodysplasia.
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PMID:Oxidative metabolism of circulating neutrophils in infantile (Philadelphia chromosome-negative) chronic myelogenous leukemia. 315 49

A megakaryoblastic cell line, termed T-33, was established from the peripheral blood of a patient with Philadelphia chromosome-positive chronic myelogenous leukemia in megakaryoblastic crisis. T-33 cells have been maintained in RPMI 1640 medium containing 10% fetal calf serum in a single cell suspension with a doubling time of 24-36 h for over 2 years. Giemsa-banded karyotypes were female hyperdiploid with a modal chromosomal number of 51, all cells including Philadelphia chromosome. The cells showed strong positivity for periodic acid-Schiff and alpha-naphthyl acetate esterase, and weak for alpha-naphthyl butyrate esterase, but were negative for myeloperoxidase. Flow cytometric analysis of cell surface markers showed the existence of HLA-DR, MY-7, MY-9, and a platelet antigen (Yukb), and no markers for T- or B-lymphocytes. Most of the cells fixed with acetone were positive for Factor VIII, platelet glycoprotein IIb-IIIa, IIIa (Yukb), and Ib, but negative for glycophorin A and hemoglobin. Ultrastructural platelet peroxidase was demonstrated in 2-3% of cells and the percentage of positive cells increased up to 20% after the treatment with 12-O-tetradecanoylphorbol-13-acetate. The cells contained small dense granules negative for platelet peroxidase, their number increasing threefold after 12-O-tetradecanoylphorbol-13-acetate treatment. Such treated cells frequently showed a complex of the demarcation membrane in the cytoplasm. T-33 responded thrombin to exhibit calcium influx. This cell line may be useful for the study of the early stage of megakaryocytic differentiation in human megakaryopoiesis.
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PMID:Establishment of a human megakaryoblastic cell line (T-33) from chronic myelogenous leukemia in megakaryoblastic crisis. 316 60

An IgG1 monoclonal antibody, 31D8, that recognizes normal neutrophil (PMN) membranes, was used to study PMN from patients with chronic myelogenous leukemia (CML). Nineteen patients with Philadelphia chromosome positive CML were followed over a ten-month period and compared with 23 normals, six patients with leukemoid reactions, and eight patients with phagocytic cell defects. The percentage of PMN binding of 31D8 among normal subjects was variable about a normal distribution with an average of 95 +/- 2% of cells binding 31D8. In contrast, there were two groups of CML patients: in 14 patients 88 +/- 3% PMN bound 31D8 while in the remaining five patients only 6 +/- 6% PMN bound 31D8. PMN 31D8 binding was normal in the control patient groups. Control antibodies 7C3 (binds to PMN precursors) and OKM1 (binds to the CR3 (iC3b) receptor) bound normally to CML neutrophils. Functionally, CML cells had normal chemotaxis to several stimuli and normal superoxide generation to phorbol myristate acetate. However, superoxide production in response to fmet-leu-phe was significantly less in 31D8 negative CML PMN than both 31D8 positive CML PMN and normal PMN which contained 85% 31D8 positive and 15% 31D8 negative PMN. Clinically, 2 of 14 CML patients with 31D8 positive PMN were in blast crisis (one extramedullary) at the time of study and the other 12 patients remained clinically stable in the chronic phase during the ten months of study. In contrast, one of five patients with 31D8 negative PMN was in blast crisis at the time of study and all four of the remaining patients progressed to either the accelerated phase or blast crisis. Three of these patients died of their disease eight to ten months after their initial study. Thus, failure of CML cells to bind 31D8 may be useful for predicting which patients are likely to progress to the accelerated phase or blast crisis.
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PMID:A neutrophil membrane marker reveals two groups of chronic myelogenous leukemia and its absence may be a marker of disease progression. 346 Jun 45

Myeloblasts from the blood of patients with chronic myeloid leukemia (CML) in a blastoid crisis were shown to have an imbalance in the ribonucleotide pools compared with normal blood neutrophils. This imbalance includes decreased ratios of purine:pyrimidine, adenine:guanine, and uracil:cytosine nucleotides as well as an increased relative concentration and a changed composition of the uridine diphosphate (UDP) sugars, with relatively more UDP-N-acetylhexosamines. Similar, more prominent deviations were found in HL-60 promyelocytic leukemia cell line cells. We have used HL-60 cells to investigate the relationships between these changes in the ribonucleotide pools and myelocyte proliferation, maturation, and/or transformation to the malignant state. When HL-60 cells were separated by elutriation centrifugation into fractions enriched in G1, S phase, or G2 + M, we found only differences in the amount of nucleotides per cell (G2 + M greater than S phase greater than G1) corresponding with the increase in cell volume but not in the qualitative composition of the nucleotides. Therefore, throughout this study, the nucleotide content of all cells was calculated per unit of cell volume. When HL-60 cells were induced to myeloid differentiation with dimethyl sulfoxide, proliferation stopped after 3 days. After 6 days, 70-90% of the cells had matured into cells capable of nitro blue tetrazolium reduction upon stimulation with phorbol myristate acetate. During the maturation process, the mean volume of the HL-60 cells decreased, and the nucleotide content and the purine:pyrimidine and adenine:guanine nucleotide ratios increased. The composition of the UDP sugars changed dramatically, with a decrease of UDP-N-acetylhexosamines and an increase of UDP-hexoses. Similar changes were detected in HL-60 cells that stopped proliferating without dimethyl sulfoxide-induced maturation, except that the UDP sugar composition showed an increase of UDP-N-acetylhexosamines and a decrease of UDP-hexoses. Careful examination of these results indicates that the decreased ratio of purine:pyrimidine nucleotides and the decreased ratio of uracil:cytosine nucleotides observed in CML myeloblasts may be regarded as specific changes caused by transformation of myelocytes to the malignant state. The increased amount of UDP-N-acetylhexosamines and total UDP sugars in the CML cells may also be connected with the transformation process. All other deviations in the nucleotide pattern of transformed myelocytes in comparison to that of mature, normal neutrophils can be explained by the state of proliferation and/or immaturity of CML myeloblasts and HL-60 cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Imbalance in the nucleotide pools of myeloid leukemia cells and HL-60 cells: correlation with cell-cycle phase, proliferation, differentiation, and transformation. 346 22

The cells from 87 leukemia-lymphoma cell lines, 14 B-lymphoblastoid cell lines, 459 cases of leukemia-lymphoma, normal specimens, 22 leukemia-lymphoma cell lines treated with 12-O-tetradecanoylphorbol 13-acetate (TPA) and 14 cases of chronic lymphocytic leukemia (CLL) and chronic myelocytic leukemia (CML) treated with TPA were analyzed for the expression of tartrate-resistant acid phosphatase (TracP) isoenzyme separated by isoelectric focusing. The TracP isoenzyme was seen in the following leukemia-lymphoma cell lines: 4 of 30 T-cell, 2 of 35 B-cell, 1 of 6 non-T/non-B-cell, 1 of 8 myelomonocytic, 3 of 4 erythroleukemia, and 3 of 4 Hodgkin's disease-derived cell lines. The expression of the TracP band could be induced by treatment with TPA in 3 myelomonocytic leukemia cell lines. Among the different types of leukemia-lymphoma cells freshly obtained from patients, the TracP isoenzyme was detected at a high incidence in cases of B-CLL, hairy cell leukemia (HCL), and B-lymphoma. Of the myeloid leukemias, 10% to 20% displayed the TracP isoenzyme. TracP positivity was detected in the peripheral blood, tonsil, bone marrow, spleen, and liver obtained from healthy donors, but not in the thymus. The expression of the TracP band could be newly induced by TPA in cases of CLL and in cases of CML. It is concluded that TracP activity is not specific for HCL, but is found at high incidences in cases of HCL, B-CLL and B-lymphoma. The TracP isoenzyme is not expressed by very immature lymphoid leukemia cells, but by cells arrested at later stages of differentiation of the T- or B-cell lineage, and by some myeloid cells.
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PMID:Occurrence of particular isoenzymes in fresh and cultured leukemia-lymphoma cells. I. Tartrate-resistant acid phosphatase isoenzyme. 348 68

The expression of a particular alpha-naphthyl acetate esterase isoenzyme which is specific for monocytes was examined in a panel of cultured leukemia-lymphoma cell lines (n = 88), freshly obtained leukemia-lymphoma cells (n = 527), and in fresh (n = 10) and cultured (n = 22) leukemia cells treated with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). The sodium fluoride-sensitive isoenzyme was separated by isoelectric focusing on horizontal thin-layer polyacrylamide gels. The esterase isoenzyme was not detected in untreated or TPA-treated lymphoid, erythroid, or Hodgkin's disease-derived cell lines, but was seen in leukemia cell lines of monocytic origin. TPA induced the new expression of this marker isoenzyme in two leukemia cell lines of promyelocytic and erythroid origin that are known to differentiate along the monocytic-macrophage cell lineage; TPA stimulation increased the staining intensity of the band in monocytoid cell lines. This esterase isoenzyme was found in 92% of the cases classified morphologically as acute myelomonocytic or monocytic leukemia, but only in 3% of the non-monocytic acute myeloid leukemias. All lymphoid or erythroid leukemias or lymphomas were negative. Treatment with TPA of AML and CML cells, which commonly differentiate to monocyte/macrophage-like cells, showed de novo the monocyte-specific isoenzyme. It is concluded that this isoenzyme is a characteristic marker for monocytic leukemia cells and will be a useful tool for the discriminatory identification of the monocytic element in normal and leukemic cells.
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PMID:Occurrence of particular isoenzymes in fresh and cultured leukemia-lymphoma cells. III. Esterase isoenzyme in monocytes. 349 69

Blood and bone marrow samples from 20 individuals with reactive conditions and 26 cases of acute and chronic myeloid leukemias were tested for the presence of lysozyme, alpha-1-antitrypsin (alpha-1-AT), and alpha-1-antichymotrypsin (alpha-1-ACT). We compared the reactivity of samples in smears, cytocentrifuge preparations, and paraffin sections. Lysozyme, alpha-1-antitrypsin, and alpha-1-antichymotrypsin were found only in polymorphonuclear leukocytes and monocytes and their precursors. Lymphocytes, E-rosetting cells, Con A-activated lymphocytes, natural killer (NK) cells, red blood cells, erythroblasts, and megakaryocytes were consistently negative. Leukemic myeloblasts showed definite reactivity for both alpha-1-antitrypsin and alpha-1-ACT, but not for lysozyme. By contrast, lysozyme was present in poorly differentiated leukemic monoblasts, while alpha-1-antitrypsin and alpha-1-antichymotrypsin showed only weak reactivity. More mature myeloid and moncytic cells showed positive staining for all three antigens tested with differences in staining distribution and intensity. In four cases of chronic myeloid leukemia (CML), circulating mature polymorphonuclear leukocytes were deficient in both lysozymne and alpha-1-antitrypsin. The use of lysozyme, alpha-1-antitrypsin, and alpha-1-antichymotrypsin identifies normal and leukemic cells of the myeloid-monocytic series at all stages of maturation and is applicable to a variety of sample preparations.
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PMID:The distribution of lysozyme, alpha-1-antitrypsin, and alpha-1-antichymotrypsin in normal hematopoietic cells and in myeloid leukemias: an immunoperoxidase study on cytocentrifuge preparations, smears, and paraffin sections. 351 16

A case of Philadelphia (Ph1) chromosome negative chronic myeloid leukaemia (CML) developed lymphoid crisis. Immunological marker studies disclosed that the lymphoid cells were sheep erythrocyte-rosetting-, Leu-1+, Leu-5+, OKT-4+, OKT-8+, common ALL antigen-, HLA-DR-, cytoplasmic and surface immunoglobulin-, MAS 036C(antithymocyte)+ (after in vitro culture) and terminal deoxynucleotidyl transferase-, indicating T-cell phenotypes, probably of common thymocytes. Cytochemical staining also demonstrated immature T-cell characters: dot-positivity for acid phosphatase and beta-glucuronidase, and negative for acid alpha-naphthyl acetate esterase. All bone marrow metaphases exhibited normal karyotypes. Our observation suggests that the neoplastic features of a common stem cell for myeloid and lymphoid cell lines are very similar in Ph1 positive and negative CMLs, and that the stem cell can differentiate towards T-lineage.
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PMID:Lymphoid crisis with T-cell phenotypes in a patient with Philadelphia chromosome negative chronic myeloid leukaemia. 387 78


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