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)

32P is effective therapy for polycythemia and primary thrombocytosis. The Polycythemia Vera Study Group is comparing radioactive phosphorus with alkylating agents to determine relative efficacy. Less well investigated is the effectiveness of 32P vs. busulfan in chronic granulocytic leukemia. Endolymphatic administration of radiopharmaceuticals may play a role in the therapy of infradiaphragmatic lymphoma. Among the radionuclides that have at times been used in hematology are 32P, 198Au 24Na, 76As, 89Sr, 52Mb, 54Mn, 91Y, 95Zr, 95Cb, 111Ag, 109Pd, 131I, 185W, and 192Ir. As stated, 32P has proven single most efficacious agent. The hematologic diseases that have been treated include both malignant and benign conditions. Among the malignant conditions are polycythemia vera, agnogenic myeloid metaplasia, thrombocythemia, leukemia, Hodgkin's disease, and multiple myeloma. Hemophilia, and Osler--Weber--Rendu disease are among the benign entities in which the agents have been tried. Polycythemia and thrombocythemia remain those in which the greatest success has been achieved.
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PMID:Radionuclide therapy of hematologic disorders. 48 47

In a group of 172 cases of polycythemia vera treated with radioactive phosphorus acute granulocytic leukemia developed in 3 and chronic granulocytic leukemia in 6 cases. The author believes that development of acute granulocytic leukemia during this treatment may be considered with some probability as a result of the leukemia-inducing action of ionizing radiation. Transition of polycythemia vera into chronic granulocytic leukemia seems to be a natural outcome of this complex myeloproliferative syndrome in patients with survival prolonged by treatment with 32P.
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PMID:Observations on polycythemia vera turning into acute or chronic granulocytic leukemia during treatment with radioactive phosphorus 32P. 106 85

The glycerolipids of most cells are characterized by a specific proportion of ether linkages at the sn-1 position of the glycerol backbone. A number of tumors are known to have altered concentrations of ether-linked lipids compared to normal tissues. However, no through examination of the ether-lipid content of human leukemia cells has been reported despite the importance of these lipids in normal leukocyte function. In the present study samples were obtained from adults with acute myelogenous leukemia (AML), chronic granulocytic leukemia in blast crisis, and acute lymphocytic leukemia and from healthy human donors. The cellular lipids were extracted, the individual phospholipid classes were isolated, lipid phosphorus content was determined, and the lipids were converted to diglyceride benzoate derivatives for separation and quantitation of the subclasses by high performance liquid chromatography. The data indicate that all the leukemic cells analyzed have an altered phospholipid composition compared to their respective normal leukocytes. Furthermore, among the AML patients both the percentage of the choline-containing phosphoglyceride fraction (PC) which is alkyl linked and the nmoles alkyl-PC/10(6) cells differ significantly by FAB subtype. A positive correlation between the levels of alkyl-PC and the degree of cellular differentiation is observed. Although no differences are observed between chronic granulocytic leukemia in blast crisis and AML lipids, the leukemic cells contain dramatically lower levels of alkyl-linked PC than do normal polymorphonuclear leukocytes. In contrast, no differences are observed between the alkyl-PC content of normal and leukemic lymphocytes. In light of the relations among ether-lipids, protein kinase C, and cell differentiation, these data suggest the ether-linked lipids are important in myeloid cell function and differentiation.
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PMID:Ether-linked phosphoglyceride content of human leukemia cells. 222 52

A dog with a myeloproliferative disorder and thrombocytosis had clinical signs that were consistent with a diagnosis of essential thrombocythemia. The dog was treated with aspirin, radioactive phosphorus, and melphalan. Eighteen months after referral, the disorder progressed to chronic granulocytic leukemia, and treatment was switched to hydroxyurea. Fourteen months later, the dog was euthanatized because of uncontrollable atrial fibrillation.
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PMID:Thrombocytosis associated with a myeloproliferative disorder in a dog. 272 42

The breakpoint cluster region gene rearrangement associated with chronic myelogenous leukemia is becoming important in the diagnosis and management of the disease. At this time, the ability to demonstrate the gene rearrangement is limited to a few research laboratories. The problem results partially from unfamiliarity of medical laboratory personnel with DNA technology, but more because of the restricted use of radiolabeled phosphorus in hospital laboratories. With the introduction of biotinylated deoxynucleotides, nucleic acid hybridization procedures can now be performed without the use of radioisotopically labeled gene probes. This article describes the use of biotin-labeled gene probes to detect the gene rearrangement of the breakpoint cluster region of chromosome 22 in chronic myelogenous leukemia. The techniques are reproducible, sensitive, and safe. With the procedures described in this article, the assay can become more available to medical laboratories interested in offering this diagnostic and decision-making tool.
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PMID:Detection of the gene rearrangement in chronic myelogenous leukemia with biotinylated gene probes. 292 2

The progression of primary thrombocythemia (PT) into acute leukemia was diagnosed in a 64-year-old man who was previously treated by hydroxyurea without alkylating agents or radioactive phosphorus. Such an event has only been reported in very rare cases. The blast cells had a lymphocytic morphology but were identified as promegakaryoblasts by the ultrastructural demonstration of platelet peroxidase. These data suggest that a megakaryoblastic transformation could occur in PT as had previously been reported in chronic granulocytic leukemia.
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PMID:Megakaryoblastic transformation of primary thrombocythemia. 393 45

The determination of N tau-methylhistamine in urine, using gas chromatography with nitrogen-phosphorus detection and the homologue N tau-ethylhistamine as internal standard, is described. A comparison between the present method and a previously described stable isotope dilution mass fragmentographic method resulted in a regression line of Y = 0.023 + 0.944X mumol/l with a correlation coefficient of 0.996. The 24-h excretions of 35 normal adults on a free diet ranged from 0.4 to 1.8 mumol. Patients with mastocytosis, chronic myelocytic leukemia, anaphylactic reactions and a patient after bronchial provocation showed above normal values.
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PMID:Determination of N tau-methylhistamine in urine by gas chromatography using nitrogen-phosphorus detection. 635 21

N tau-Methylimidazoleacetic acid, the quantitatively most important metabolite of histamine, was isolated from urine by ion exchange chromatography. After esterification with 2-propanol and extraction, N tao-methylimidazoleacetic acid was analyzed by capillary gas chromatography with nitrogen-phosphorus detection, using N tao-ethylimidazoleacetic acid as internal standard. The synthesis of this internal standard is described. In contrast to the methods hitherto described, this method is appropriate for use in clinical chemical laboratories. Normal 24-h excretion ranged from 8.3 to 18.5 mumol (n = 20). Five patients with mastocytosis, a patient with chronic myelocytic leukemia and a patient after an anaphylactoid reaction on acetylsalicylic acid showed highly elevated values.
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PMID:Determination of N tau-methylimidazoleacetic acid (a histamine metabolite) in urine by gas chromatography using nitrogen-phosphorus detection. 695 73

Two patients with chronic myeloid leukemia (CML) presenting with the hematologic features of essential thrombocythemia (ET) are reported. At diagnosis they showed extremely high platelet counts (4985 and 2800 x 10(9)/l, respectively) and moderate leukocytosis (21 and 17 x 10(9)/l, respectively). In both cases, in addition to the Philadelphia chromosome (Ph), a rearrangement within the major breakpoint cluster region on chromosome 22 was demonstrated, with the breakpoint in the 3' extreme. In patient 1 the disease initially responded to radioactive phosphorus and hydroxyurea, but during the evolutive course a progressive increase in the white blood cell counts was noted, reaching values typical of the chronic phase of CML, and the patient eventually died from blast crisis 45 months after diagnosis. In patient 2, although good control of the platelet counts was achieved with hydroxyurea, the disease also evolved into a blast crisis four months after diagnosis. In both cases monoclonal antibodies and electron microscopy studies demonstrated the megakaryocytic nature of the blast cells. The above features are not consistent with the present and similar cases being Ph-positive ET. Instead, they should be regarded as a special form of CML characterized by a marked protagonism of the megakaryocytic component.
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PMID:Ph-positive chronic myeloid leukemia mimicking essential thrombocythemia and terminating into megakaryoblastic blast crisis: report of two cases with molecular studies. 842 85

Myeloproliferative disorders (MPD) are prone to modification and evolution during the progression of the disease. While post-polycythemia myeloid metaplasia and chronic myelogenous leukemia following polycythemia vera have been frequently described, no report is available about the evolution of polycythemia vera into essential thrombocythemia. Our case is probably the first report on this occurrence. In the course of a fortuitous observation of electrocardiographic alterations, a diagnosis of polycythemia vera was ruled out in accordance with polycythemia vera study group criteria. At the time of diagnosis, RBC was 6 x 10(12)/L, WBC 15 x 10(9)/L, Ht 59% and platelets 1000 x 10(9)/L. The patient was treated with phlebotomies and radioactive phosphorus achieving a good remission or the disease. Five years later, platelets rose to over 3300 x 10(9)/L without significant modification or RBC, WBC and Ht. The restaging or the disease was consistent for an essential thrombocythemia. In particular, RBC mass was within normal levels. During the last ten years, the patient has been followed recurrently and the blood picture remained stationary, without an increase in the hematocrit but with a platelet count between 658 and 800 x 10(9)/L. We conclude that this report may complete data concerning the evolution of MPD in others.
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PMID:Essential thrombocythemia following polycythemia vera: an unusual sequence. 915 Dec 4


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