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)

Platelet activation in patients with myeloproliferative disorders is often suggested by increased platelet alpha-granule secretion and an acquired storage pool defect of dense granules. To determine whether activated platelets circulate in patients with chronic myeloproliferative disorders, we evaluated the binding of monoclonal antibodies against activation-dependent epitopes on resting platelets (P 12, CD 63, and CD 62) in 12 patients with prominent megakaryocytic proliferation (8 patients with essential thrombocythemia, 2 with chronic myeloid leukemia, and 2 patients with polycythemia rubra vera). In addition, platelet aggregation in response to collagen, adenosine diphosphate, platelet activating factor, and agglutination with ristocetin was investigated. In 3 patients there was an increased percentage of platelets binding at least 1 activation marker. In 2 other patients, a trend towards increased antibody binding was observed. Binding of the antibody to thrombospondin (P 12) was related to expression of the GMP 140 protein (CD 62, r = 0.76, p = 0.004). There was no correlation of platelet aggregation defects in vitro to increased expression of platelet activation markers or to thrombohaemorrhagic complications. However, circulating activated platelets were detected in three out of five patients with a history of bleeding or thrombotic complications. The results of this preliminary study suggest that some but not all patients with myeloproliferative disorders showed increased amounts of circulating activated platelets. The relation of bleeding and thrombotic complications to the expression of activation-dependent epitopes on platelets in myeloproliferative disorders requires further investigation.
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PMID:Circulating activated platelets in myeloproliferative disorders. 170 9

A case of essential thrombocythemia with a partial deletion of the long arm of chromosome 11, del(11)(q21) as a sole chromosomal anomaly is reported. Rearrangement of chromosome 11 at band 11q21 has been reported in six patients with chronic myeloproliferative disorders: four with post-polycythemic myelofibrosis, one with myelofibrosis with myeloid metaplasia, and one with Ph+ chronic myeloid leukemia in blastic phase. Except for the last patient, all patients had been treated with 32P and/or an alkylating agent prior to cytogenetic examination. This is the first report of the 11q21 abnormality in essential thrombocythemia seen at diagnosis.
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PMID:Chromosome 11 rearrangement at band 11q21 in a patient with essential thrombocythemia. 172 43

Enzyme negative blast cells from 27 patients with chronic myeloproliferative disorders (CMPDs) in blastic transformation were analysed with a panel of monoclonal antibodies (MoAbs). According to morphologic features of the bone marrow and laboratory data, the 27 cases were divided into 8 cases of myelofibrosis (MF), 3 cases of chronic megakaryocytic granulocytic myelosis (CMGM) and 16 cases of chronic myeloid leukaemia (CML). Of the 27 cases, 23 showed a positive reaction with myeloid MoAbs, but in 12 cases expressing myeloid markers, megakaryocytic, monocytic or lymphoid cell features were also detected. In 7 cases of MF, 1 case of CMGM and 1 case of CML a bilineage, myelo-megakaryocytoid immunophenotype of peripheral blast cells was seen. Of the 4 patients with CML expressing lymphoid markers, 2 showed early B-cell, 1 T-cell surface antigens, and 1 both myeloid and early B-cell features. In this group of cytochemically immature blastic transformation of CMPD, only 1 case was termed "undifferentiated" blastic transformation.
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PMID:Enzyme negative blastic transformation of chronic myeloproliferative disorders: immunophenotyping of the blastic cell population. 181 60

Cytogenetic findings were correlated to histopathological bone marrow findings evaluated simultaneously in 103 patients with chronic myelogenous leukemia (CML). CML was subtyped histologically according to the number of megakaryocytes and increase of fibers or blasts within the bone marrow. The Philadelphia chromosome (Ph 1) was found in 88.3% of all patients (91/103). Chromosome aberrations additional to the Ph 1-chromosome were noticed in 20 of 91 (22%) cases. The additional karyotype changes occurred significantly more frequently among patients with increase of fibers in the bone marrow compared with patients without increase of fibers or blasts (p less than 0.05). Karyotype changes associated with increase of fibers in Ph 1-positive cases of CML were trisomy 8 and 19, +Ph1, t (1; 11), and i (17q). Ph 1-positive CML patients with additional karyotype changes had a significantly shorter survival (p less than 0.04) than Ph 1-positive patients without additional chromosome aberrations. Our results suggest that histopathological examination of the bone marrow should be considered in the evaluation of cytogenetic markers in chronic myeloproliferative disorders.
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PMID:Cytogenetics of chronic myelogenous leukemia (CML) correlated to the histopathology of bone marrow biopsies. 193 98

One hundred and seventy bone marrow biopsies from patients with chronic myeloproliferative disorders (CMPDs) were evaluated for the presence of lymphoid nodules (LNs) and were immunostained using a panel of monoclonal antibodies (UCHL1, 4KB5 and L26) recognizing different lymphocyte antigens. LNs were found in 35% of cases of idiopathic thrombocythaemia, 24.6% of myelofibrosis/osteomyelosclerosis, 18.2% of polycythaemia vera 12.1% of chronic myeloid leukaemia and 19.2% of borderline cases. Varying degrees of immunohistochemical positivity for the three antibodies tested were found. LNs were always made up of variable proportions of both T- and B-lymphocytes with a prevalence of T-cells. This latter observation suggests that bone marrow LNs in CMPDs could be an expression of reactivity.
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PMID:Immunohistochemical evaluation of bone marrow lymphoid nodules in chronic myeloproliferative disorders. 194 8

Bone marrow stroma was investigated immunohistochemically in 31 patients with haematological diseases, mainly idiopathic myelofibrosis (n = 8) and related chronic myeloproliferative disorders (n = 14). The bone marrow from patients with idiopathic myelofibrosis and some CML patients showed marked staining reactions with antibodies against type III procollagen (pN collagen), type IV collagen, fragment P1 of laminin and factor VIII. Patients with osteomyelosclerosis had particularly increased collagen content, including both newly deposited type III collagen (pN collagen) and mature collagen fibres. As in normal bone marrow, argyrophilic fibres and type III collagen displayed a close co-distribution, which was also demonstrated for type IV collagen and laminin. While normal bone marrow sinusoids had discontinuous basement membranes, fibrosing bone marrow was characterized by endothelial cell proliferation and capillarization, with the development of continuous sheets of basement membrane material beneath endothelial cells.
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PMID:Bone marrow stroma in idiopathic myelofibrosis and other haematological diseases. An immunohistochemical study. 200 Dec 83

A morphometric evaluation of number and grouping of megakaryocytes (MK) in five different groups of chronic myeloproliferative disorders (CMPD) was performed by counting 60 high power fields equaling approximately 14.28 mm2 of haematopoiesis in each case. Twenty-one up to 29 cases were evaluated for each of five categories of CMPD and one control group; a total of 132 cases of CMPD and 33 control cases were used. The mean number of MK per square millimetre was 15.54 +/- 1.53 in chronic myeloid leukaemia of common or granulocytic type (CML.CT), 69.91 +/- 5.85 in CML with megakaryocytic increase (CML.MI), 59.59 +/- 3.27 in polycythaemia vera (P. vera), 59.85 +/- 4.59 in primary thrombocythaemia (PTH), 67.58 +/- 4.11 in chronic megakaryocytic granulocytic myelosis (CMGM), and 19.7 +/- 3.07 in controls. The distinction between free or isolated MK, and between clustered or grouped MK corresponds to the total cell counts of MK in the various groups of CMPD. Clustering of MK was significantly higher in CMGM and PTH compared to other groups, but the difference between them was not statistically significant. Significant differences in the mean number of MK were obtained between controls and CML.CT on the one hand and all other groups of CMPD on the other. The results further support the histological sub-classification of CMPD according to the primary disorders of the Hannover classification (not advanced by sclerosis, fibrosis or excess of blasts, respectively).
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PMID:Megakaryocytes in chronic myeloproliferative disorders: numerical density correlated between different entities. 205 83

Numeric and planimetric parameters of megakaryocytes have been analyzed in 162 bone marrow biopsies of patients with chronic myeloproliferative disorders--CMPD--and controls by means of an inductive knowledge-based system in combination with a multivariate data analysis. To achieve a reliable differential diagnosis between the different entities of CMPD and controls, decision trees and the rank order of the best discriminating parameters have been calculated. The cases measured were defined by 3 histopathologists who were involved in the elaboration of the Hannover Classification of CMPD. The results demonstrate striking numeric and morphologic characteristics of the megakaryopoiesis in each separate primary category of CMPD, that is (1) chronic myeloid leukemia of the common type and (2) with megakaryocytic increase, (3) polycythemia vera, (4) primary or idiopathic thrombocythemia, and (5) chronic megakaryocytic-granulocytic myelosis. Thus, the morphometric measurements did confirm the validity of the Hannover Classification of CMPDs. In order to evaluate the information contained in large quantitative and semiquantitative data bases and diagnostic decisions, knowledge-based expert systems seem to represent a valuable addition to conventional statistics.
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PMID:Quantitative cytomorphology of megakaryocytes in chronic myeloproliferative disorders--analysis of planimetric and numeric characteristics by means of a knowledge based system. 209 68

This Diagnostic Seminar intends to announce that CMPDs can be classified from BMB histologically by a rather simple system, which can be applied by interested histopathologists successfully. The rationale of this classification is to stay within the groups of diseases which are outlined by clinical findings including the peripheral blood and bone marrow smears. The concept of traditional classification as given by the WHO and textbooks, however, has to be revised as follows (1) Primary diseases of CMPDs must be distinguished from advanced disorders. Primary diseases are CML, P. vera, Thrombocythemia, CMGM, and unclassifiable CMPD. (2) Idiopathic, primary myelosclerosis of the bone marrow is a reactive feature consecutive to neoplastic transformation of hematopoiesis, i.e. myeloproliferation. (3) Advanced disorders comprise (3.1.) excess of blasts and blast crisis, and (3.2.) early myelosclerosis, myelosclerosis and myelofibrosis, advanced myelofibrosis. Advanced disorders are designated by a composed term classifying them among the groups of primary disease and specifying the advanced stage by a suffix, so that the underlying disease remains coining the term, even in unclassifiable cases in which only CMPDs can be applied. (4) The CML group must be subtyped into CML of common type versus that with increase or predominance of megakaryocytes. By this system of classification, it seems possible to classify and type the spectrum of variations occurring among CMPDs to a satisfying result.
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PMID:Chronic myeloproliferative disorders in bone marrow biopsies. 217 9

Leukocytosis, mild anemia, thrombocytosis, and panhyperplasia in the marrow characterize the early stages of most of the CMPD, whereas extramedullary hematopoiesis (such as in the spleen or liver), peripheral cytopenias (anemia, leukopenia, or thrombocytopenia), and myelofibrosis, with or without osteosclerosis, reflect the changes seen in the later stages. Transitions among the different CMPD and termination in acute leukemia or marrow failure also are common. CML often is characterized by leukocytosis and the presence of the entire spectrum of granulocytes (mature and immature) in the blood and marrow, reduced LAP, hypercellularity with prominent granulocytic hyperplasia in the marrow, Ph chromosome, and bcr-abl gene rearrangement. Typical features of AMM include leukoerythroblastosis, teardrop poikilocytosis, anemia, increased or normal LAP, prominent megakaryocytic hyperplasia in the marrow, dyshematopoiesis, and hyperplastic or fibrotic/sclerotic marrow.
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PMID:Myeloproliferative disorders. Classification and diagnostic features with special emphasis on chronic myelogenous leukemia and agnogenic myeloid metaplasia. 227 76


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