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)

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

Recurrent bilateral leg ulcers developed in two patients receiving hydroxyurea therapy during the chronic phase of chronic myelogenous leukemia. The ulcers were extremely painful and were associated with extensive edema and vasculitic papules. A small-vessel vasculitis with degeneration of collagen and ulceration was seen on biopsy. The ulcers did not respond to treatment with steroids or low-dose cyclophosphamide but gradually healed with local measures. The possible pathogenesis of ulcers in chronic myelogenous leukemia is discussed.
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PMID:Vasculitic leg ulcers in chronic myelogenous leukemia. 385 57

Biopsy specimens of skin from 42 patients with leukemia cutis were studied. Typing of leukemia was based on histopathologic and histochemical findings in peripheral blood and bone marrow. There were three patients with acute lymphocytic leukemia, 16 with chronic lymphocytic leukemia, 12 with acute granulocytic leukemia, three with chronic granulocytic leukemia, five with acute monocytic leukemia, and three with acute myelomonocytic leukemia. In general, leukemia cutis shows a diffuse infiltration of leukemic cells in the dermis and subcutaneous tissue, often infiltrating between collagen bundles. Extensive involvement and disruption of blood vessels and skin adnexa are characteristic findings in granulocytic, monocytic, and myelomonocytic leukemia cutis, but biopsy specimens of skin in patients with different types of leukemia show a wide range of histopathologic changes that are variable among the various types of leukemia and sometimes even among different patients with the same type of leukemia. A final typing of leukemia should not rely only on regular histopathologic findings of a skin biopsy, but should depend more on morphologic and histochemical studies of smears of peripheral blood or of bone marrow or both.
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PMID:Leukemia cutis. A histopathologic study of 42 cases. 386 Nov 7

Bone marrow obtained at autopsy from four cases of primary myelofibrosis and four cases of chronic myelogenous leukemia, was studied electron microscopically. In all the cases of primary myelofibrosis, the excess of collagen fibers in the bone marrow showed mostly about 2,000 A diameter and 1,000 A periodicity, i.e. fibrous long spacing (FLS)-like fibers. These FLS-like fibers were also seen in secondary myelofibrosis in three of the four cases of chronic myelogenous leukemia. These fibers were abundant around fibroblasts and small blood vessels. An apparent continuity between the dark bands of FLS-like fibers and the basement membrane material around small blood vessels was also revealed. Moreover, it was observed that these dark bands of FLS-like fibers contained acid mucopolysaccharides.
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PMID:Fibrous long spacing-like fibers in the bone marrow of myloproliferative disorder. 612 34

In a preliminary manner, the data presented here characterize some features of MSC and their progenitors. The progenitors, at least in chronic myelogenous leukemia, are derived from the neoplastic pluripotent stem cell that also differentiates along lymphoid and myeloid pathways. In addition, we have demonstrated that the precursor for MSC is lacking both the Ia and CALLA determinants. Several antigenic and functional characteristics of the mature stromal cell population have also been identified. Stromal cells express CALLA, synthesize types I, III, and IV collagen, and may express factor VIII associated antigen. It is of interest that fibroblasts do not express factor VIII associated antigen, do not synthesize type IV collagen in measurable quantities, but do express CALLA [9]. Endothelial cells express factor VIII associated antigen, synthesize type IV collagen, but are not CALLA positive. Thus, MSC have some features in common with fibroblasts and others with endothelial cells. The unique characteristics of MSC are that they are transplantable and are derived from a common progenitor with other hematopoietic cells. These features clearly distinguish this cell population from fibroblasts, which are neither transplantable nor derived from the neoplastic clone in CML.
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PMID:Studies on the in vitro microenvironment in man. 634 89

In 9 patients with myeloproliferative diseases (MPD) (6 with myelofibrosis, MF, 1 with Ph1 positive chronic granulocytic leukaemia, CGL, 1 with primary eosinophilia, PE, 1 with pre-leukaemia syndrome, preL) collagen, epinephrine, and ADP-induced aggregation, N-ethylmaleimide-induced malondialdehyde (MDA) production, beta-thromboglobulin (beta-TG) plasma levels, and platelet turnover were studied. Collagen-induced aggregation was found to be normal in 7 patients, absent in 1, and reduced in 1. In all but 3 patients, aggregation with ADP was markedly reduced. Epinephrine-induced aggregation was decreased in 7 patients. No difference was found between mean MDA production in MPD (3.21 +/- 0.50 nmol/10(9) PLTs) and in control group of 21 normal subjects (3.04 +/- 0.26 nmol/10(9) PLTs). Mean beta-TG levels were significantly higher (P less than 0.01) in MPD patients (165.00 +/- 28.29 ng/ml) than in healthy controls (81.76 +/- 14.63 ng/ml). Mean platelet production half-time was significantly shorter in MPD (2.48 +/- 0.24 d) than in the control group (3.43 +/- 0.17 d), after adjustment for age by covariance analysis (P less than 0.005). Our data do not indicate an abnormal prostaglandin synthesis and are consistent with the hypothesis that a disseminated intravascular platelet aggregation might take place in MPD patients.
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PMID:Defective platelet aggregation and increased platelet turnover in patients with myelofibrosis and other myeloproliferative diseases. 646 Oct 58

Platelet aggregation was studied in 18 patients with myeloproliferative disorders, including 14 patients with chronic myelogenous leukemia, 2 with polycythemia vera, 1 with myelofibrosis and 1 with thrombocythemia. Fourteen patients (78%) were abnormal in epinephrine-induced platelet aggregation, while 3 (17%) and 4 (22%) cases showed impaired ADP or collagen induced platelet aggregation, respectively. A significant decrease of total ADP content in resting unstimulated platelets and of the amount released to the medium after aggregation was found in all six patients who were evaluated. ATP and AMP in resting platelets tended to be slightly higher in patients compared with the control group. Released ATP was also significantly less, and the percentage release of ADP and ATP was significantly decreased in patients. A storage pool deficiency of adenine nucleotides was considered to be responsible for abnormal platelet function in patients with myeloproliferative disorders.
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PMID:Abnormalities of epinephrine-induced platelet aggregation and adenine nucleotides in myeloproliferative disorders. 653 53

A new type of acquired platelet dysfunction was found in a chronic myeloid leukaemia patient with petechiae and thrombocytosis. Platelet aggregation induced by arachidonic acid (AA), collagen and A23187 was decreased, secondary aggregation by ADP and epinephrine was defective and ristocetin-induced aggregation was completely reversible. No platelet ATP was released by AA and collagen. Only high concentrations of AA (greater than or equal to 2 mM) induced minimal reversible aggregation. 14C-serotonin uptake by the platelet and platelet adenine nucleotide contents were normal. Normal AA metabolism was demonstrated by thin-layer radiochromatographic analysis of the metabolites of 14C-AA and the determination of thiobarbituric acid reactive substances produced by the incubation of AA or thrombin with the platelets. Minimal reversible aggregation was observed when patient's platelet-rich plasma was added to a reaction mixture in which thromboxane A2 (TXA2) had been generated. TXA2 produced by patient's platelets showed normal platelet-aggregating activity. These results suggest that a subnormal platelet response to TXA2 is included as a mechanism for this acquired hypofunction of the platelet.
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PMID:Subnormal platelet response to thromboxane A2 in a patient with chronic myeloid leukaemia. 680 32

Chronic myeloproliferative disorders (MPD) are clonal diseases of the pluripotent hematopoietic stem cell frequently associated with myelofibrosis (MF). There is only indirect evidence indicating that the increased deposition of collagen in bone marrow matrix is a secondary phenomenon. A liquid culture system for cloning and growing bone marrow fibroblasts has permitted us to approach more directly the understanding of the pathogenesis of myelofibrosis by comparing the biophysical, growth, and functional characteristics of fibroblasts from normals, MPD patients without MF, and those with MF. In patients with MF, marrow fibroblast colony (CFU-F) formation could not be studied; fibroblasts were grown from marrow explants. CFU-E from normals and MPD patients exhibited similar cell density distribution and similar cell sedimentation rates. These similarities contrasted sharply with the differences seen when the erythroid and granulocyte-macrophage progenitors were studied by the same methods. There was a marked light density shift and a rapidly sedimenting shift of MPD hematopoietic colony-forming cells. Marrow fibroblasts from MPD patients with and without MF displayed the same in vitro growth characteristics as fibroblasts from normals. Both types of fibroblasts exhibited anchorage and serum dependence, and contact inhibition of growth. Marrow fibroblasts were also characterized for the presence and distribution of fibronectin and collagen types by immunofluorescent staining using monospecific antibodies. Extracellular matrix, membrane-, and cytoplasm-associated fibronectin, type I, type III, and type V collagen showed a similar staining pattern in both normal and myelofibrotic marrow fibroblasts. Plasminogen-dependent fibrinolytic activity elicited from normal and myelofibrotic marrow fibroblasts were equivalent. Chromosomal analysis of hematopoietic cells and marrow fibroblasts from Philadelphia chromosome positive chronic myelocytic leukemia patients with and without MF showed that the Philadelphia chromosome was present only in hematopoietic cells. The results of these studies taken together demonstrate that bone marrow collagen-producing cells from MPD patients with and without MF behave in vitro as do those from normals. These findings support the hypothesis that that the marrow fibrosis observed in patients with MPD results from a reactive process rather than from a primary disorder affecting the marrow collagen-producing cells.
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PMID:Characteristics of bone marrow fibroblast colony-forming cells (CFU-F) and their progeny in patients with myeloproliferative disorders. 704 2

Several platelet abnormalities have been described in myeloproliferative diseases. The present study deals with 81 patients with polycythaemia vera, chronic myelogenous leukemia, essential thrombocythaemia and idiopathic myelofibrosis, and reports the analysis of the findings in platelet-induced aggregation. Platelet abnormalities induced by ADP, adrenaline and collagen were found in 41.9% of the patients. A defect of primary aggregation was documented in 13 cases and one of them showed an aggregation pattern similar to that of Glanzmann's disease. Fifteen patients had an impairment of secondary aggregation, and in one case of this group the platelet malondialdehyde and serotonin findings were consistent with a defect resembling that of typical congenital storage pool deficiency. A disturbance of the arachidonic acid pathways associated with a storage pool deficiency was found in a third patient belonging to a group with abnormalities of primary and secondary aggregation. In conclusion, platelets in myeloproliferative diseases have several defects and in a few cases their combination is similar to those of congenital diseases.
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PMID:Spectrum of platelet aggregation abnormalities in myeloproliferative diseases. 722 3


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