Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new method of detecting the C3b receptor is reported. A particular merit of this method is that anti-RBC rabbit antiserum is not required. Rosettes were formed with human B lymphocytes, B lymphoblasts and granulocytes, using sheep erythrocytes (SRBC) sensitized with fresh human serum (FHS). T lymphocytes and T lymphoblasts did not form rosettes. The percentage of cells forming rosettes with this method approximated the percentage of rosettes formed with EACm. However, FHS coated SRBC did not react with most cells of B cell type chronic lymphocytic leukemia (CLL), whereas EACm rosette formations showed a definite reaction. On the other hand, 34--58% of cells of chronic myelocytic leukemia (CML) bound with the indicator red cells. SRBC sensitized with fresh rabbit or guinea pig serum formed rosettes with PBL, tonsil cells, B lymphoblasts and granulocytes. Complement and IgM antibody were required for this reaction, as in EAC rosette formation.
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PMID:Detection of human B cells and chronic myelocytic leukemic cells by rosette formation with sheep erythrocytes and fresh human sera. 31 33

The investigations, performed to study the possible mechanism of action of PTC, of its single constituents and of meta-levo-sarcolysin (m-L-SL) on the human immunocompetent system, are reported. The study entailed the evaluation of the effect of PTC, of its peptides and of m-L-SL on the various lymphocyte classes, employing all the more sophisticated immunological techniques such as: a) lymphocyte cultures stimulated with the various mitogens, (T and B lymphocytes); b) E rosettes (T lymphocytes); c) EA rosettes (lymphocytes with Fc receptors for IgG); d) EAC rosettes (lymphocytes with the C3 receptors); e) autoradiography and intracytoplasmic immunofluorescence (in vitro immunoglobulin neosynthesis); f) CdL (Complement-dependent Lymphocytotoxicity); g) LALI (Lymphocyte Antibody Lymphocytolytic Interaction); h) CML (antibody independent cytotoxicity i.e. Cell-Mediated Lympholysis). The evidence points out that the PTC effect on T and B lymphocytes is not comparable to that of m-L-SL which does not discriminate between the two lymphocyte populations while PTC, besides showing a scarce immunodepressive effect, preferentially affects B lymphocytes rather than T lymphocytes as shown also by the E rosette pattern. Significantly different appears also the influence of PTC, as compared with that of m-L-SL on the lymphocytes with Fc receptors for IgG (EA rosettes) and with receptors for the third component of complement (EAC rosettes) as well as on the cytotoxicity test and on the antibody dependent (LALI) and complement dependent (CdL) lytic effect. The data gleaned from this investigation allow evaluating both the effects of PTC on the immunocompetent system and the difference of its action from that of m-L-SL.
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PMID:Effects of an antitumor multipeptide complex on immunocompetent and antigen-responsive cells. 108 83

A 42-year-old male with chronic myelogenous leukemia (CML) developed acute transformation associated with subcutaneous tumors. Histopathologic examinations of the tumors were done on two occasions; the first study revealed reticulum cell sarcoma-like features, and the second suggested a blastoma. Chromosomal analysis showed that the cells of the tumors originated from the CML clone. The cells had a negative reaction for myeloperoxidase by electron microscopy. Furthermore, biochemical and surface marker studies revealed that the tumor cells contained a significant terminal transferase activity. However, they did not express E- or EAC-rosette receptors, Ia-like antigens, or common ALL antigens.
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PMID:Characterization of extramedullary tumors in a case of Ph-positive chronic myelogenous leukemia: possible involvement of immature T lymphocytes. 387 50

The osmotic behavior of control lymphocytes (CL) and polymorphonuclears (CPMN) was compared with that of cells from patients with chronic lymphocytic leukemia (CLL) and chronic myelocytic leukemia (CML), using the method of gradual dialysis against distilled water. The results were evaluated with a fragiligraph, and by scanning (SEM) and transmission (TEM) electron microscopy. The fragiligraphy curves showed that CLL cells are more resistant to osmotic pressure than the CL, whereas the curves for CPMN and CML cells showed an overlap. Surface alterations in CL appeared as early as 1 min of dialysis, while in CLL cells the membrane did not show major alterations even after 5 min of dialysis. CPMN also showed alterations earlier than CML cells, but this difference was not as prominent as in the case of lymphocytes and was observed for a maximum of 3 min of dialysis. The internal structure of the cells was altered earlier than the surface membrane and this was expressed mainly in the nucleus in both control and leukemic cells. Also in this respect, the internal structure of CL was altered earlier than that of CLL cells, whereas no major differences were observed between CPMN and CML cells.
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PMID:SEM and TEM studies on the osmotic behavior of control and leukemic lymphocytes and polymorphonuclears. 612 53

Leukemic cells from 32 patients were examined by using conventional immunological markers (E and EAC rosettes, surface immunoglobulins). Additionally, the test for intracytoplasmic IgM, Fc IgG receptor and the presence of light chains were performed. Leukemic blasts of all patients were investigated according to morphological and cytochemical criteria. Lymphoblasts from 3 patients had pre-B cell phenotype: cIgM +, sIg-. Each of 3 patients with pre-B cell characteristics had different diagnosis and different morphological and cytochemical features of the leukemic cells (ALL, NHL and CML). In 24 ALL cases the diagnosis of non-T, non-B ALL, in 4 cases T-ALL and in one B-ALL was established. The correlation of cytochemical results with special reference to acid phosphatase and immunological subclasses of ALL was also analyzed. An important question is raised with regard to diagnostic classification and treatment by finding ALL phenotypes in lymphoproliferative disorders that are not diagnosed as ALL.
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PMID:Immunological typing of blast cells. Cases with pre-B cell characteristics. 620 92

Lymphocytes from 22 patients with chronic myeloid leukemia (CML), 13 treated with polychemotherapy, eight by monochemotherapy, and one untreated, were analyzed for the presence of classic T and B cell surface markers (E-rosette, EAC-rosette, surface immunoglobulins) and for their ability to respond to phytohemagglutinin (PHA). The absolute number and percentage of E-rosetting cells (T-cells), EAC-rosetting cells and cells staining for surface immunoglobulins (B cells) were all significantly lower than controls (P less than or equal to 0.025). The response to PHA was also significantly lower in patients than in controls at the smaller concentrations of the mitogen (3.75 micrograms/ml, 30 micrograms/ml) tested (P less than or equal to 0.01); at a higher PHA concentration (120 micrograms/ml) the decrease in PHA stimulation approached significance (P = 0.07). These lymphocyte abnormalities support the concept that CML lymphocytes may be derived from the leukemic clone.
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PMID:Cell membrane markers and phytohemagglutinin reactivity of circulating lymphocytes from chronic myelocytic leukemia patients. 694 3

Normal and neoplastic human hematopoietic cells were examined for surface markers by a variety of techniques including cytotoxicity assays using anti-HTLA and anti-Ia antiserum with viability measured by trypan blue exclusion and automated flow cytometry; E- and EAC-rosette binding assays and surface immunoglobulin measured by a fluorescence-activated cell sorter. In most cases there was good agreement among these assays. However, one case of CLL of T origin (92% E-rosette-positive) also showed significant amounts of Ia antigen by cytotoxicity tests; additionally, a case of CML in blast crisis demonstrated no E or EAC markers or surface immunoglobulin, but the majority of cells were lysed by both anti-HTLA and anti-Ia antiserum. Thus, Ia is not an exclusive B cell marker.
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PMID:Flow cytometric analysis of normal and neoplastic human hematopoietic surface antigens. 700 54

The bactericidal activity of polymorphonuclear leucocyte (PMNL) against infection stimulates cytoskeletal changes accompanied with alteration in adhesion and locomotion. Microfilaments, the motile apparatus is known to regulate these changes by polymerization of monomeric G-actin to fibrous F-actin. PMNL from chronic myeloid leukemia (CML) patients have been reported to be defective in locomotion in response to synthetic peptide, n-formyl-methionyl-leucyl-phenylalanine (fMLP) but the mechanism leading to defective locomotion and their spatial reorganization remains unclear. Therefore, in order to study the cause of defective motility of PMNL from CML patients the spatial distribution and reorganization of microfilaments and microtubules in response to fMLP have been examined by transmission electron (TEM) and scanning electron microscopy (SEM). Under SEM, the PMNL-CML surface appeared smoother with reduced ruffling resulting in rounding off cells with lesser polarized morphology. Unstimulated PMNL from normal as well as CML subjects showed shorter and fewer microtubules and evenly distributed microfilaments as compared to fMLP stimulated PMNL. It is proposed that the cause of defective locomotion was due to reduced surface activity as a consequence of altered cytoskeletal configuration. This phenomenon seems to be related to impaired functional appendages and as a whole led to the defective cell motility and hence reduced chemotaxis in PMNL from CML patients.
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PMID:Impaired cell motility in chronic myeloid leukemic granulocytes related to altered cytoskeletal pattern. 1653 57

Leukemic patients of different classifications are associated with anemia. Such clinical conditions are often referred to as refractory anemia, paraoxymal nocturnal hemoglobinuria, hemolytic uremia and autoimmune hemolytic anemia, all of which could be categorized as the cancer cachexia. In the present work, we have studied the overall morphology of intact red cells in different leukemic patients along with patients of hypoplastic anemia (HPA) by scanning electron microscopy. We have also studied the ultrastructure of the red cell surface membranes by transmission electron microscopy. For all experiments, erythrocytes from normal individuals served as controls. We have shown direct evidence of the altered red cell (RBC) membrane morphology irrespective of the hemoglobin status of the patients which includes (1) presence of large central holes in RBCs of acute myeloid leukemia (AML), (2) presence of thorn- and horn-like structure in RBCs of acute lymphoblastic leukemia (ALL) and chronic myeloid leukemia (CML) and (3) flaccid appearance of RBCs in chronic lymphocytic leukemia (CLL) patients. A mixture of the above mentioned structures were found in the red cells of patients suffering from myelodysplastic syndrome (MDS) and in case of patients of HPA the RBCs lost the normal biconcave structures. TEM studies revealed presence of pores with diameters ranging from 100 to 200nm on the RBC membrane surface of myeloid leukemia with AML being the most prominent among others. Such pathophysiological alterations of the RBC morphology in leukemic patients could be identified as characteristic signature of the onset of anemia associated with the disease.
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PMID:Red cell morphology in leukemia, hypoplastic anemia and myelodysplastic syndrome. 1687 91

Here we describe the purification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) from normal leukocytes of healthy subjects and leukocytes of chronic myeloid leukemia (CML) patients and from normal mouse muscle and sarcoma tissue. The data indicate that some properties of GAPDH of leukocytes of CML patients and sarcoma tissues are similar and also similar to those of EAC (Ehrlich ascites carcinoma) cellular GAPDH but distinctly different from those of the normal cellular GAPDH. Polyclonal antiserum raised against the 54 kDa subunit of EAC cell GAPDH strongly reacted with GAPDH of leukocytes of CML patients and sarcoma tissue GAPDH only and weakly reacted with GAPDH of normal leukocyte and normal muscle and a variety of other tissues of normal rats. Both the subunits of GAPDH of sarcoma tissues were partially sequenced from the N-terminus and compared with the known sequences of GAPDH. The altered properties of GAPDH of three different malignant sources might be common feature of all malignant cells, which is discussed in relation to glycolysis and malignant aberrations.
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PMID:Molecular characterization of tumor associated glyceraldehyde-3-phosphate dehydrogenase. 1974 91


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