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)

Determining granulocyte kinetics with DF32P allows various parameters to be gained during the in-vitro marking, such as the total blood granulocyte pool, circulating granulocyte pool, marginal granulocyte pool, daily granulocyte exchange rate and half decay period of granulocytes. The half decay period of granulocytes, bone-marrow reserve in myelocytes, metamyelocytes and band cells as well as polymorphonuclear neutrophils can be determined by in-vitro marking, with DF32P being intravenously injected. The combination of both procedures with DF32P will reveal the half decay period, pool sizes and exchange rates of the proliferating myelocyte compartiment in bone-marrow and mature blood granulocytes. If 51Cr is used for determining granulocyte kinetics the surface activities of various organs, such as heart, liver, spleen, and lungs, can mainly be determined in addition to the half-life of leucocytes, indicating the degradation or storage of cells in certain areas of the body. In addition to normal values those findings are principally presented which were obtained with in-vitro marking by DF32P and 51Cr in chronic myeloid leukaemia, osteomyelofibrosis or osteomyelosclerosis respectively and in hypersplenism.
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PMID:[Granulocyte kinetics with radioactive diisopropylfluorophosphate (DF32P) and radiochrome (51Cr)]. 8 82

Two male patients with myeloproliferative disorders (osteomyelosclerosis in one and CML in the other) were found to have a chromosomal marker 20q- in blood cells (unstimulated short time cultures). Marked erythropoietic disturbances were not revealed in these cases. The specificity of the 20q- marker for red cell disorders is discussed.
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PMID:Chromosomal marker 20q- in cases of osteomyelosclerosis and CML. 28 24

Since the discovery of a very high blood histamine level in chronic myelocytic leukemia (CML) 1936, the author could ascertain that this parameter is very useful in the differential diagnosis between CML and various "leukemoid" reactions; in the early diagnosis of CML and in the differential diagnosis between CML and other myeloproliferative disorders. Recent researches proved that no correlation exists between blood histamine level and basophil count in the peripheral blood. Further investigations in this field have to clear up the questions whether it is possible by means of repeated controls of the blood histamine level to predict the development of a polycythemia vera into CML or to establish in a case of osteomyelosclerosis that this disease has been Preceeded by A CML.
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PMID:[Blood histamine level in chronic myeloproliferative diseases; a review]. 39 72

A histological study on sequential bone marrow biopsies in patients with chronic myeloid leukaemia (CML) was performed. We wished to answer the question as to whether a different content of megakaryopoiesis in the bone marrow of CML patients has a prognostic significance for the development of myelofibrosis during the course of disease. In addition, the significance of possible changes in the quantity of megakaryopoiesis in this process was assessed. In 186 patients who had no fibre increase at first diagnosis, the rate of subsequent myelofibrosis varied from 19% for the common or granulocytic subtype (CML.CT) to 40% for patients with features of megakaryocytic increase (CML.MI). No significant differences were found either in the rapidity of progression to fibrosis or in the final rate of osteomyelosclerosis. Whereas in CML.MI most patients (75%) showed an increase of fibres only, this was accompanied by an additional increase of megakaryocytes in CML.CT, changing the histological pattern from CML.CT to .MI or .MP, respectively. The data therefore revealed a correlation between fibre increase and subtyping of CML as suggested by the Hannover classification of chronic myeloproliferative diseases. Subtypes of CML with megakaryocytic increase could be shown to present a "pre-myelofibrotic" stage of disease and may therefore be conceived as a particular pathway of acceleration.
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PMID:The impact of megakaryocyte proliferation of the evolution of myelofibrosis. Histological follow-up study in 186 patients with chronic myeloid leukaemia. 160 7

An immunohistochemical and morphometric study was performed on routinely processed trephine biopsies of the bone marrow in 30 normal individuals and in 90 patients with various subtypes of chronic myeloproliferative disorder. Using a new monoclonal antibody (PG-M1) directed against a formalin-resistant epitope on macrophages and by employment of the Prussian blue reaction, quantitation of this cell population was feasible. Morphometric analysis revealed that the number of iron-laden macrophages represented only a fraction of the total number of histiocytic reticular cells. As could be expected, in polycythaemia rubra vera, no haemosiderin deposits were detectable, but the content of macrophages slightly exceeded that of the normal bone marrow. In chronic myeloid leukaemia 9 of 30 patients showed a significant increase in PG-M1-positive reticular cell elements. These were consistent with pseudo-Gaucher cells, sea-blue histiocytes and intermediate cell types. Primary (idiopathic) myelofibrosis-osteomyelosclerosis was characterized by a significant increase in macrophages (25 of 30 patients). Involvement of macrophages in the complex mechanisms generating bone marrow fibrosis and angiogenesis and in bone remodelling (osteosclerosis) may be responsible for this finding.
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PMID:Macrophages in normal human bone marrow and in chronic myeloproliferative disorders: an immunohistochemical and morphometric study by a new monoclonal antibody (PG-M1) on trephine biopsies. 163 47

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

Serum ferritin concentration was studied in 79 patients with chronic granulocytic leukemia (CGL), 14 patients with polycythemia vera (PV), eleven patients with osteomyelosclerosis (OMS) and four patients with megakaryocytic myelosis (MM). Pretreatment serum ferritin concentrations were found to be normal or slightly decreased in patients with PV, OMS, MM and in the chronic phase of CGL. Patients entering the blastic crisis of CGL had highly increased serum ferritin concentrations. The severity of hyperferritinemia in these patients depended on the cytomorphological type of the blastic crisis. Highest levels of serum ferritin concentration were found in the immature myeloblastic type according to the M1- and M2-type of the FAB-classification of acute leukemias (i.e. 30-fold and 18-fold increased). In contrast, the rise of the serum ferritin concentration in the more mature types of blastic crisis was less pronounced (i.e. nine-fold in the M3-type and six-fold in the M4- and M5-type of blastic crisis). Patients with complete remission after bone marrow transplantation had normal serum ferritin concentrations. Investigation of the intracellular ferritin concentration showed, that the serum ferritin levels paralleled the intracellular ferritin concentration within the leukemic blasts: During the myeloic blastic crisis the intracellular ferritin concentration was found to be 17-fold increased compared to the intracellular ferritin concentrations in the chronic phase of CGL. Thus, our data support the concept that an increased synthesis of ferritin by the leukemic blasts is responsible for the increased serum ferritin concentration during the blastic crisis of CGL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ferritin in myeloproliferative diseases]. 233 46

Mononuclear cells from the peripheral blood of healthy test persons were cultivated in a methylcellulose medium with serum samples taken from 13 patients with chronic myeloid leukemia (CML) and with osteomyelosclerosis (OMS) as well as with serum samples of 6 healthy test persons. From evaluating the proliferation of granulopoietic cells quantitatively, conclusions were made concerning the concentrations of granulopoietic stimulating substances in these sera. In all cultures with the serum of patients the number of granulopoietic cell colonies was greater than that in cultures with the serum of normal persons. The stronger proliferation of granulopoietic precursor cells in cultures with serum of patients is seen to be due to an enhanced production of the granulocyte-macrophage colony stimulating factor (GM-CSF) by leukemic cells. The differential hemograms and curves indicating the course of leukocytes in patients are compared with the corresponding results of cultures. In patients with CML an increased output of GM-CSF will apparently influence the increase in size of the granulopoietic stem cell pool, which is evident in the steep increase of those curves indicating the course of leukocytes. In patients with OMS, however, there is a discrepancy between granulopoietic serum activity and proliferation in vivo. From these investigations the hypothesis is derived that an increased synthesis of GM-CSF in patients with CML may be one of the causes underlying hyperplastic granulopoiesis. A direct advantage of leukemic cells in proliferation cannot be derived from it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum factors in chronic myeloid leukemia]. 241 18

The total urinary hydroxyproline excretion was assessed in 47 patients with chronic myeloproliferative disorders. Urinary hydroxyproline excretion was normal in 16 patients with idiopathic myelofibrosis and in 5 out of 6 patients with acute myelofibrosis. In patients with osteomyelosclerosis (n = 8) values for urinary hydroxyproline excretion were higher (median 202, range 54-652) than those in idiopathic myelofibrosis (median 139, range 84-216). This difference was not significant (p greater than 0.1). Elevated values for urinary hydroxyproline excretion were found in 10 patients (1 AMF patient, 3 OMS patients and 6 patients with CML in the accelerated phase of the disease). All but 1 of these patients had been treated, or were being treated, with cytotoxic agents at the time of investigation. These findings are compatible with impaired degradation of bone marrow collagen which, together with enhanced collagen synthesis from bone marrow fibroblasts, accounts for progressive accumulation of connective tissue in the bone marrow. This process appears to be influenced by cytotoxic treatment as reflected in increased urinary hydroxyproline excretion in those patients receiving cytotoxic agents.
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PMID:Urinary hydroxyproline excretion in the myelofibrosis-osteomyelosclerosis syndrome and related diseases. 369 62


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