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 chromosomal anomaly, 21q-, has been found in association with retroviral indicators in patients with myeloproliferative disorders (MPD) including polycythemia vera (PV), essential thrombocythemia (ET), chronic myelocytic leukemia (CML) and acute non-lymphocytic leukemia (ANLL). The viral indicators are found in platelet homogenates of thrombocythemic patients. Evidence is presented from 2 laboratories (Philadelphia, USA and Bologna, Italy) for the 21q- deletion in MPD patients. Thirty patients evaluated for the presence of both viral and chromosomal markers in Philadelphia showed positive correlations.
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PMID:Correlation of a specific chromosomal marker, 21q-, and retroviral indicators in patients with thrombocythemia. 9 52

Platelet lipoxygenase and cyclo-oxygenase pathways were investigated by the incubation of 1(-14) C-arachidonic acid with washed platelets in 33 patients with myeloproliferative disorders, including 14 patients with chronic myeloid leukemia (CML), 12 with polycythemia vera (PV), 4 with essential thrombocythemia (ET), and 3 with myelofibrosis (MF). In patients with MF and CML, mean activities of the lipoxygenase pathway were significantly lower when compared with normal controls (p less than 0.001 and p less than 0.01, respectively). When a normal range of the activity was defined as mean +/- 2 SD, all patients with MF, 8 with CML, 6 with PV, and 1 with ET showed decreased lipoxygenase activities, while activities of the cyclo-oxygenase pathway were decreased in one of each patient with CML, PV, and ET. In 4 of 10 patients with a selective lipoxygenase deficiency, platelets were aggregated by lower concentrations of arachidonic acid than those necessary to induce normal platelet aggregation. It is suggested that the lipoxygenase activity could modulate platelet functions through its effect on arachidonate metabolism by the cyclo-oxygenase pathway and that a selective lipoxygenase deficiency could offer a mechanism for hyperfunction of the platelet, which may lead to a thrombotic tendency, one of the common features of myeloproliferative disorders.
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PMID:Altered arachidonate metabolism by platelets in patients with myeloproliferative disorders. 11 95

Myeloproliferative disease of childhood is frequently associated with chromosomal anomalies, usually of the C group. Clinical features are similar to those of the juvenile type of chronic myeloid leukemia. A child with this disease is described. Marked myeloid proliferation, anemia, thrombocytopenia and hepatosplenomegaly were present; leukocyte alkaline phosphatase and fetal hemoglobin were moderately elevated. Chromosome analysis of bone marrow cells revealed a mosaicism 47,XX,+21/46,XX. Down's syndrome was ruled out by the child's normal phenotype and dermatoglyphic analysis. The cytogenetic finding is probably evidence for the clonal origin of the trisomy 21 cell line.
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PMID:Myeloproliferative disease of childhood associated with a trisomy 21 clone. 11 7

Three cases of myeloproliferative disorders in patients with breast cancer are described. The first patient developed acute myeloblastic leukemia 26 years after her initial breast cancer; the second patient developed chronic myelogenous leukemia three years after the diagnosis of breast cancer; the third patient had polycythemia vera for nine years before cancer of the breast was noted. The literature dealing with the association of cancer and myeloproliferative disorders is reviewed. Possible explanations for this association are considered.
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PMID:Association of breast cancer with myeloproliferative disorders. 19 48

Prostaglandin (PG) D(2) is synthesized in platelets at concentrations which could inhibit aggregation via activation of adenylate cyclase. To more directly define platelet-PG interactions, a binding assay has been developed for platelet PG receptors with [(3)H]PGD(2) as ligand. [(3)H]PGD(2) binding to intact platelets was saturable and rapid with the ligand bound by 3 min at 20 degrees C. PG competed with the [(3)H]PGD(2) binding site with a potency series: PGD(2) (IC(50) = 0.08 muM) >> PGI(2) (IC(50) = 2 muM) > PGE(1) (IC(50) = 6 muM) > PGF(2alpha) (IC(50) = 8 muM). Scatchard analysis of binding data from six normal subjects showed a single class of binding sites with a dissociation constant (K(d)) of 53 nM and 210 binding sites per platelet. This PGD(2) receptor assay was then used to study platelets from five patients with myeloproliferative disorders (polycythemia vera, essential thrombocythemia, and chronic myelogenous leukemia), as over 90% of these patients have platelets resistant to the effects of PGD(2) on aggregation and adenylate cyclase activity (1978. Blood.52: 618-626.). In the presence of 50 nM [(3)H]PGD(2), the patients' platelets bound 7.1+/-2.9 fmol ligand/10(8) platelets compared with 15.1+/-1 fmol/10(8) platelets in normals, a decrease of 53% (P < 0.01). Scatchard analysis showed that the K(d) of [(3)H]PGD(2) binding (33 nM) was comparable to normal platelets, which indicates that the decreased PGD(2) binding in these platelets represented fewer receptors rather than altered affinity of the ligand for the binding site. The 53% decrease in [(3)H]PGD(2) binding correlated with a 48% decrease in PGD(2)-activated platelet adenylate cyclase. The characterization of the platelet PGD(2) binding site provides further direct evidence that there are at least two PG receptors on platelets, one for PGE(1) and PGI(2), and a separate receptor for PGD(2). Direct binding analysis will be a useful tool for studying the role of PG in regulating platelet function, as demonstrated by the selective loss of PGD(2) binding sites in patients with myeloproliferative disorders.
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PMID:Characterization of the platelet prostaglandin D2 receptor. Loss of prostaglandin D2 receptors in platelets of patients with myeloproliferative disorders. 22 13

A combination of eight cytotoxic drugs, administered simultaneously, has been used in 86 cases of acute leukemia. The regimen, designated TRAMPCOL, incorporated thioguanine, rubidomycin, (daunorubicin), cytosine arabinoside, methotrexate, prednisolone, cyclophosphamide, vincristine, and usually L-asparaginase. Treatment was administered in five-day pulses with treatment-free intervals varying from nine to 23 days. Subjective and objective toxic effects were not more severe than those seen with two- and four-drug regimens previously employed. Substantial clinical and hematologic improvement occurred in 8/19 patients with chronic granulocytic leukemia (CGL) in acute transformation. Complete clinical and hematologic remission (CR) was achieved in 3/7 patients with untreated acute myeloid leukemia (AML), 5/19 patients with AML who had failed to achieve CR with other therapy, and 4/18 patients with AML in relapse after CR obtained with regimens other than TRAMPCOL. CR occurred in 15/17 patients with acute lymphocytic leukemia (ALL), most of whom had had multiple previous relapses. CR was not achieved in four patients with AML superimposed on pre-existing myeloproliferative disorders. The TRAMPCOL regimen merits further evaluation in CGL after acute transformation, as a primary treatment for AML, and as therapy for ALL 1) in relapse, 2) in adults, 3) in children with adverse prognostic features, and 4) in T-cell ALL.
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PMID:Multiple-drug chemotherapy for acute leukemia The TRAMPCOL regimen: results in 86 patients. 26 3

Pyoderma gangrenosum (PG) has been increasingly reported in association with myeloproliferative disorders. Monoclonal gammaopathy, myeloma, myeloid metaplasia, and polycythemia have all been found in association with PG. Recently, seven cases of PG in association with leukemia have been described: three cases with acute myeloblastic leukemia, two cases with chronic myelogenous leukemia, one case with acute lymphoblastic leukemia, and one case with acute leukemia of either plasma cell or myeloblast origin. To these we add two cases of PG with acute myeloblastic leukemia. These patients often have an atypical clinical presentation for PG, with bullae and relatively superficial involvement obscuring the correct diagnosis.
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PMID:Atypical pyoderma gangrenosum with leukemia. 27 73

Antiserum raised in rabbits against the FBP obtained from CML cells, and the purified binder labeled with 125I, have been used for an RIA which can measure an immunologically similar protein in human serum. The concentration of the binding protein in normal serums ranged from 1.2 to 9.3 ng/ml, with a mean +/- S.E.M. of 3.8 +/- 0.4 ng/ml. Elevated values of the binder protein were measured in the serums from patients with folate deficiency, vitamin B12 deficiency, liver disease, uremia, myeloproliferative disease, chronic lymphocytic leukemia, and various types of cancer and in the serum from pregnant women. The concentration of the binder protein and the capacity of the serum to specifically bind isotopically labeled PGA correlated poorly, indicating that the binding protein concentration and degree of saturation by endogenous serum folate vary independently in many instances.
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PMID:The identification and measurement of a folate-binding protein in human serum by radioimmunoassay. 27 99

Forty patients with various types of myeloproliferative disorders were evaluated immunologically. Serum immunoglobulin levels were within the normal range in most patients and no monoclonal gammopathies were detected. Serum C'3 levels were decreased in 19 of 40 (48%) patients. The response of peripheral blood lymphocytes to phytohemagglutinin was decreased in 26 of 40 (65%) and to pokeweed mitogen in 18 of 28 (64%) patients studied. Lymphocytes from patients with polycythemia vera were least affected. Unstimulated lymphocytes from some patients demonstrated markedly increased thymidine uptake activity. Despite the diminished mitogenic response, only 2 of 33 patients (6%) were anergic by intradermal skin testing. There was no association between depressed lymphocyte response and recent chemotherapy except in chronic myelogenous leukemia where 6 of 8 patients were receiving cytotoxic therapy when studied. These observations suggest that most of our patients with myeloproliferative disorders have abnormal cellular responses in vitro, but that delayed hypersensitivity and humoral responses are minimally affected.
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PMID:Immunologic dysfunction in the myeloproliferative disorders. 27 12

An experimental model system is presented for the investigation in humans of the role of hematopoietic stromal elements in the regulation of hematopoiesis as well as in the pathogenesis of myelofibrosis in myeloproliferative disorders. The model is based on the simultaneous application of three experimental techniques: (1) growth of bone-marrow derived fibroblastic colonies in vitro, (2) cytogenetic demonstration of marker chromosomes associated with hematopoietic malignancies, and (3) the transplantation of isolated stromal elements into athymic (nude) mice. Using this model, we describe the induction of mesenchymal tumors in nude mice by Ph1 negative fibroblasts obtained from the bone marrow of a patient with a Ph1 positive chronic myelogenous leukemia. Mesenchymal tumors also were induced in nude mice with bone marrow-derived fibroblasts from a patient with aplastic anemia, who was successfully treated with bone marrow transplantation, and from a normal human volunteer. Morphologic, cytogenetic and electron microscopic studies of bone marrow mesenchymal elements in culture and of tumors induced in nude mice from the CML patient indicate the cells composing the tumor are of human origin and are negative for the Ph1 chromosome. The results provide the first in vivo morphological and cytogenetic support using human materials, of the hypothesized relationship of progenitors of in vitro fibroblastic colonies to marrow stromal elements.
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PMID:Production of mesenchymal tumors in nude mice by Ph1 negative fibroblasts obtained from a Ph 1 positive CML patient: a preliminary report. 27 72


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