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)

We investigated the hemorheological, hematological and biochemical parameters in 30 cases of acute lymphocytic leukemia (ALL), 21 cases of acute myelogenous leukemia (AML) and 30 cases of chronic myelogenous leukemia (CML). The parameters studied include whole blood viscosity, plasma viscosity, erythrocyte sedimentation rate (ESR), red cell filterability, hematocrit, platelet count and aggregation, fibrinogen, hemoglobin, leucocyte count, bleeding time and lactate dehydrogenase activity (LDH). In the cases of ALL we observed significant decrease in whole blood viscosity, hemoglobin, hematocrit and platelet count but an increase in plasma viscosity, fibrinogen, bleeding time and LDH activity. In the cases of AML, we observed increase in whole blood viscosity, plasma viscosity, ESR, fibrinogen, leucocyte count, bleeding time and LDH activity but decrease in the hemoglobin, hematocrit and platelet count. In the cases of CML, we observed an increase of whole blood viscosity, plasma viscosity, ESR, fibrinogen elevation but decreases in bleeding time. In all cases, red cell filterability was unaffected.
Physiol Chem Phys Med NMR 1992
PMID:Blood viscosity parameter correlation with types of leukemia. 150 91

The effect of hydroxyurea on blood viscosity was studied in 10 patients with Philadelphia chromosome positive chronic myelogenous leukemia (CML) and hyperleukocytosis (white blood cell counts over 200 x 10(9)/l). All the patients had visible manifestations of leukostasis such as headache, blurred vision, retinal hemorrhage, pulmonary infiltrates, etc. Contraves LS 30 viscometer was used to measure the blood viscosity at 37 degrees C and at different shear rates on paired leukemic blood samples obtained before and after the hydroxyurea treatment. The blood viscosity was significantly higher in CML patients then normal subjects and decreased after treatment with hydroxyurea. In all the cases plasma viscosity was unaffected by the treatment.
Physiol Chem Phys Med NMR 1991
PMID:Effect of hydroxyurea on blood viscosity in chronic myelogenous leukemia with hyperleukocytosis. 181 5

This study was carried out to investigate the red blood cell and white blood cell deformability index in leukemia which is marked by an uncontrolled increase of leucocytes in the bone marrow as well in peripheral blood. It was observed that leucocytes are less deformable than erythrocytes, and erythrocytes from Chronic Myelogenous Leukemia (CML) patients less deformable than normal erythrocytes. The deformability indexes for lymphoblasts from acute lymphoblastic leukemia and myeloblasts from acute myelogenous leukemia were almost the same and higher than that of granulocytes from chronic myelogenous leukemia. These observations led to the conclusion that the significant increase in the resistance to the flow of blood in vivo in leukemia may be due to the increase in the number of leucocytes which are more rigid than erythrocytes.
Physiol Chem Phys Med NMR 1993
PMID:Cellular deformability studies in leukemia. 815 54

In-vivo 31P-NMR spectroscopy of the spleen was carried out in 15 patients with splenomegaly from various causes (Hodgkin's disease, non-Hodgkin lymphoma, polycythaemia vera, chronic lymphatic leukaemia, chronic myeloid leukaemia). Volume selection was with the ISIS technique, voxel size was between 3 x 5 x 5 and 8 x 6 x 7 cm3. There was a markedly elevated (PM+Pi)/beta-NTP quotient (mean 3.41 with a standard deviation of 0.37) (p < 0.001) and raised PDE/beta/NTP quotient as compared with 8 normals, who showed an (PME+Pi)/beta-NTP quotient of 2.32 and a PDE/beta/NTP quotient of 1.11. These raised quotients were interpreted as indicating increased membrane phospholipid metabolism due to increased cell turnover. The data suggest there may be some clinical value in performing 31P-NMR spectroscopy for defining splenic involvement in myeloproliferative diseases but further confirmatory studies will be necessary.
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PMID:[Initial results of in vivo 31P-NMR spectroscopy of the spleen in patients with splenomegaly]. 835 66

The hematopoietic cellular kinase (Hck) is a member of the Src family of non-receptor protein-tyrosine kinases that is expressed predominantly in granulocytes, monocytes and macrophages. Recent observations suggest that Hck may be activated in HIV-infected macrophages and in chronic myelogenous leukemia cells that express Bcr-Abl. In order to increase our understanding of the structural basis for regulation of Hck activity under normal and pathological conditions, we have solved the solution structure of the uncomplexed Hck SH2 domain using NMR spectroscopy. A novel procedure that uses intraresidue HN-H alpha distances as references for converting NOE intensities into distance restraints has been described. A total of 1757 significant experimental restraints were derived from NMR spectroscopic data including 238 medium-range and 487 long-range distance restraints and 177 torsion angle restraints. These restraints were used in a simulated annealing procedure to generate 20 structures with the program DYANA. Superimposition of residues 5-104 upon the mean coordinate set yielded an average atomic rmsd values of 0.42 +/- 0.08 A for the N,C alpha,C' atoms and 0.81 +/- 0.08 A for all heavy atoms. Rmsd values for those residues in the regions of ordered secondary structure were 0.27 +/- 0.04 A for the N,C alpha,C' atoms and 0.73 +/- 0.06 A for all heavy atoms.
J Biomol NMR 1997 Oct
PMID:Three-dimensional structure of the Hck SH2 domain in solution. 939 Apr 4

Two new modified uracil nucleosides, 5-carbamoylmethyuridine (ncm5U, I) and 5-carbamoylmethyl-2-thiouridine (ncm5s2U, II) were isolated from a 24 hr collection of a normal human urine. The structures were assigned on the basis of UV, NMR and mass spectral data and confirmed by comparison of the spectral data and HPLC mobilities with those of authentic samples. On the basis of experimental data it appears possible that 5-carbamoylmethyl-2-thio-uridine (ncm5s2U, II) may be a degradation product produced from a labile precursor by the chemical treatments during the isolation procedure. However, the other nucleoside (ncm5U,I) certainly appears to be of metabolic origin and was also found in the urines of one chronic myelogenous leukemia and one lung carcinoma patient. Abbreviations used are: tRNA-transfer ribonucleic acid, TMS-trimethylsilyl, RP-HPLC--reverse phase high performance liquid chromatography, EI--electron impact, cm5U-5-carboxymethyluridine, mcm5U-5-methoxycarbonylmethyluridine, cm5s2U-5-carboxymethyl-2-thiouridine, mcm5s2U-5-methoxycarbonylmethyl-2-thiouridine, t6A-9-beta-D-ribofuranosyl-[N(purin-6-yl)carbamoyl]-1-threonine, C-cytidine, acp3u-3-(3-amino-3-carboxypropyl)uridine, AICR-aminoimidazole carboxamide riboside, alpha-4-PCNR & beta-4-PCNR-9-alpha-D-(or beta-D)-ribofuranosyl-pyridin-4-one-3-carboxamide, H x 7R-7-beta-D-ribofuranosyl hypoxanthine, m3U-3-methyluridine, m1I-1-methylinosine, m1G-1-methylguanosine, DI-5'-deoxyinosine, dms5OA-5'-deoxy-5'-methylthioadenosine sulfoxide, m2(2)G-N2-dimethylguanosine, psi-psi-uridine, A-adenosine, I-inosine, CML-chronic myelogenous leukemia mam5s2U-5-methylaminomethyl-2-thiouridine, ncm5U-5-carbamoylmethyluridine, ncm5s2U-5-carbamoylmethyl-2-thiouridine, UV-ultraviolet, NMR-nuclear magnetic resonance, HPLC-high performance liquid chromatography, GC-MS-gas chromatography-mass spectrometry.
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PMID:Isolation and characterization of 5-carbamoylmethyluridine and 5-carbamoylmethyl-2-thiouridine from human urine. 1061 23

Magnetic resonance images of leukemic bone marrow were acquired over large regions of the pelvis and lower abdomen with minimal interference from overlying tissues using diffusion and T(2) weighted echo planar imaging. Data acquisition times were on the order of 1 min for scanning volumes of up to 25 l at a spatial resolution of 31 microl. A survey of 21 patients with leukemia and eight healthy adult volunteers was undertaken to determine the magnitude of the observed effect and its dependence upon specific pathologies. The acquisition methods yielded high-quality segmentation of leukemic bone marrow prior to therapy in seven of seven patients with acute lymphocytic leukemia, chronic lymphocytic leukemia or chronic myelogenous leukemia, and who had hypercellular (>95%) bone marrow at the time of the study. The quality of the segmentation was sufficient to allow the use of maximum intensity projection images which afforded a convenient evaluation of both intra- and extramedullary disease. The measured signal-to-noise ratios agreed with a theoretical estimate that accounted for the percentage cellularity, T(2) relaxation time of water, and self-diffusion coefficient of water in iliac bone marrow. In addition, the mean signal-to-noise ratios from iliac marrow were strongly dependent upon the time after the initiation of chemotherapeutic regimens, implying that the methods may be useful for therapeutic monitoring.
NMR Biomed 2000 Oct
PMID:Bone marrow segmentation in leukemia using diffusion and T (2) weighted echo planar magnetic resonance imaging. 1100 12

The new square-planar Pt(II) and Pd(II) complexes with cytokinin-derived compounds Bohemine and Olomoucine, having the formulae [Pt(BohH(+))Cl(3)].H(2)O (1), [Pt(Boh)(2)Cl(2)].3H(2)O (2), [Pt(Boh-H)Cl(H(2)O)(2)].H(2)O (3), [Pt(OloH(+))Cl(3)].H(2)O (4), [Pd(BohH(+))Cl(3)].H(2)O (5), [Pd(Boh)Cl(2)(H(2)O)] (6), [Pd(Boh-H)Cl(H(2)O)].EtOH (7) and [Pd(OloH(+))Cl(3)].H(2)O (8), where Boh=6-(benzylamino)-2-[(3-(hydroxypropyl)amino]-9-isopropylpurine and Olo=6-(benzylamino)-2-[(2-(hydroxyethyl)amino]-9-methylpurine, have been synthesized. The complexes have been characterized by elemental analyses, IR, FAB+ mass, 1H, 13C and 195Pt NMR spectra, and conductivity data. The molecular structure of the complex [Pt(BohH(+)-N7)Cl(3)].9/5H(2)O has been determined by an X-ray diffraction study. Results from physical studies show that both Bohemine and Olomoucine are coordinated to transition metals through the N(7) atom of purine ring in all the complexes. The prepared compounds have been tested in vitro for their possible cytotoxic activity against G-361 (human malignant melanoma), HOS (human osteogenic sarcoma), K-562 (human chronic myelogenous leukemia) and MCF-7 (human breast adenocarcinoma) cell lines and IC(50) values have been also determined for all the complexes. IC(50) values estimated for the Pt(II)-Bohemine complexes (2.1-16 microM) allow us to conclude that they could find utilization in antineoplastic therapy. Thus, from a pharmacological point of view, Pt(II) complexes of Bohemine may represent compounds for a new class of antitumor drugs.
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PMID:Mixed ligand complexes of platinum(II) and palladium(II) with cytokinin-derived compounds Bohemine and Olomoucine: X-ray structure of [Pt(BohH+-N7)Cl(3)].9/5H2O [Boh=6-(benzylamino)-2-[(3-(hydroxypropyl)-amino]-9-isopropylpurine, Bohemine]. 1266 1

Five ORFs were detected in a fragment from the Streptomyces venezuelae ISP5230 genomic DNA library by hybridization with a PCR product amplified from primers representing a consensus of known halogenase sequences. Sequencing and functional analyses demonstrated that ORFs 11 and 12 (but not ORFs 13-15) extended the partially characterized gene cluster for chloramphenicol (Cm) biosynthesis in the chromosome. Disruption of ORF11 (cmlK) or ORF12 (cmlS) and conjugal transfer of the insertionally inactivated genes to S. venezuelae gave mutant strains VS1111 and VS1112, each producing a similar series of Cm analogues in which unhalogenated acyl groups replaced the dichloroacetyl substituent of Cm. 1H-NMR established that the principal metabolite in the disrupted strains was the alpha-N-propionyl analogue. The sequence of CmlK implicated the protein in adenylation, and involvement in halogenation was inferred from biosynthesis of analogues by the cmlK-disrupted mutant. A role in generating the dichloroacetyl substituent was supported by partial restoration of Cm biosynthesis when a cloned copy of cmlK was introduced in trans into VS1111. Complementation of the mutant also indicated that inactivation of cmlK rather than a polar effect of the disruption on cmlS expression had interfered with dichloroacetyl biosynthesis. The deduced CmlS sequence resembled sequences of FADH2-dependent halogenases. Conjugal transfer of cmlK or cmlS into S. venezuelae cml-2, a chlorination-deficient strain with a mutation mapped genetically to the Cm biosynthesis gene cluster, did not complement the cml-2 lesion, suggesting that one or more genes in addition to cmlK and cmlS is needed to assemble the dichloroacetyl substituent. Insertional inactivation of ORF13 did not affect Cm production, and the products of ORF14 and ORF15 matched Streptomyces coelicolor A3(2) proteins lacking plausible functions in Cm biosynthesis. Thus cmlS appears to mark the downstream end of the gene cluster.
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PMID:Biosynthesis of the dichloroacetyl component of chloramphenicol in Streptomyces venezuelae ISP5230: genes required for halogenation. 1470

The site-specific basicities of imatinib (Gleevec, a new signal transduction inhibitor drug of chronic myeloid leukemia) and two of its fragment compounds were quantitated in terms of protonation macroconstants, microconstants, and group constants by NMR-pH and pH-potentiometric titrations. Sequential protonation of imatinib follows the N(34), N(11), N(31), N(13) order, in which N(11) and N(31) show commensurable basicity, but negligible intramolecular interaction. Fragment compounds include two "halves" of imatinib, and their moiety-specific basicities confirm the NMR-based protonation sequence of the parent compound. NMR-pH profiles, macro- and/or microscopic protonation schemes, and species-specific distribution diagrams are presented. On the basis of these data, imatinib is shown to be predominantly neutral, monocationic, and tricationic at intestinal, blood, and gastric pH, respectively. The molecular hypotheses on imatinib binding to the Bcr-Abl oncogene fusion protein are interpreted at the site-specific level in view of the moiety basicities of imatinib.
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PMID:Acid-base profiling of imatinib (gleevec) and its fragments. 1563 18


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