Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dynamical changes in the spleen of mice and rats were studied morphometrically and electron microscopically when the animals were given in drinking water radionucleotides in small concentrations (137Cs, 226Ra, 89Sr, 65Zn, Pb(NO3)2, BeCl2, hexamethyleniamine, methylmercurchloride) for 1-2 years. Total doses obtained for a year were 0.3-100 rad. Reactive reconstruction of the organ under radioactive and chemical effects was stated to proceed in three directions: a) hyperplasy of lymphoid tissue; b) enhanced plasmocytogenesis; c) hyperplasy of extramedullar hemopoiesis. Sequence in the appearance of these reactions and doses which produced them were different for every compound. In 1-2 years at large doses (160-200 rad) atrophy, amyloid degeneration of the spleen or signs of leukemia were observed. Disturbance of intercellular contacts and of intracellular regeneration was demonstrated electron microscopically.
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PMID:[Effect of various non-radioactive and radioactive chemical compounds on the structure of the spleen]. 67 27

A quick and quantitative evaluation technique, "AgNORs-FCM", was developed to analyze Nucleolar Organizer Regions (NORs) stained with silver impregnation followed by cytofluorometric analysis. Cell suspension is stained with AgNORs similarly as described elsewhere for tissue sections, but with a modification of using a much lower concentration of silver nitrate. Cytological general rules in AgNORs-FCM are: 1) Specific exaggeration of side scatters (90 LSs) can be detected according to the intensity of AgNORs staining. 2) Significantly brighter 90 LSs were observed when cultured leukemia cell-line was applied to AgNORs-FCM. 3) AgNORs-FCM provides more specifically brighter 90 LS for cells in G2M and S phase, when gated along the P.I.-fluorescence. AgNORs-FCM can be applied to analyze clinico-pathological samples including neoplastic tissues, more quickly and quantitatively, than regular tissue staining with AgNORs.
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PMID:[AgNORs (Ag nucleolar organizer regions)]. 144 4

Four cases of metastatic calcification due to hypercalcemia in adult T-cell leukemia-lymphoma (ATLL) are reported. Serum calcium was at high levels, 15.4-19.4 mg/dl (normal range 8.4-10.4 mg/dl). In our cases, metastatic calcification was detected by v. Kossa's silver nitrate method for calcium in tubules of kidneys (100%), pulmonary alveolar septa of lungs (100%), myocardium (75%), muscular layer of stomach (50%), lower portion of aortic media (50%), gastric mucosa (25%), testicular tubules (25%), and in the liver (25%). Scattered osteoclasts were seen around the cortex of the bone. Therefore, hypercalcemia in ATLL may have been caused by bone-resorption-stimulating factors which promote differentiation of osteoclast cells, resulting in calcium increase in the serum.
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PMID:Metastatic calcification due to hypercalcemia in adult T-cell leukemia-lymphoma (ATLL). 176 85

Vinblastine or colchicine, administered intraperitoneally to B6D2F1 mice with advanced subcutaneous colon 38 tumours, induced substantial tumour growth delays with progressive development of haemorrhagic necrosis beginning within 8 hours of treatment. Two multidrug-resistant P388 leukaemia sublines, refractory to vinblastine and vincristine when grown as intraperitoneal ascites, were sensitive to necrosis induction when grown as subcutaneous tumours. Vascular labelling with two fluorescent markers indicated that vincristine substantially reduced tumour blood flow within 4 hours after treatment. The effects of vinblastine, vincristine and colchicine were similar to those of tumour necrosis factor alpha in that: (a) similar tumour necrosis and blood flow changes were induced, (b) coadministration of the serotonin antagonist cyproheptidine prevented tumour necrosis and (c) plasma nitrate levels were elevated, indicative of the stimulation of oxidation of L-arginine to nitric oxide. The results suggest that vinca alkaloids and colchicine act on solid tumours by host cell-mediated vascular effects as well as by direct tubulin-mediated cytotoxicity.
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PMID:Inhibition of growth of colon 38 adenocarcinoma by vinblastine and colchicine: evidence for a vascular mechanism. 182 25

Immediate allergy is caused by a chemical mediator released from basophile and mast cells via cell degranulation due to reaction between an immunoglobulin E (IgE) antibody, bound with the IgE receptor on the cell membrane, and an antigen. The present authors have established a new method for assaying the enzyme activity of beta-hexosaminidase as an index of chemical mediator release. Using cultured cells instead of conventional methods based on histamine release from mast cells, the present method permits highly accurate mass screening since it uses a well-established cell line of rat basophilic leukemia cells (RBL-2H3). The effects of metal elements on immediate allergic reaction were evaluated using a newly developed assay system. A total of 38 metal elements were investigated for effects on immediate allergic reactions in vitro. These elements were classified by five types on the basis of action on beta-hexosanimidase release: 1) those which showed very strong inhibitory action, such as ZnCl2 and ZrCl4, 2) those which showed relatively strong inhibitory action, such as CdCl2 and CuCl2, 3) those which showed relatively weak inhibitory action, such as CoCl2 and Pb(NO3)2, 4) those which showed neither inhibitory nor promoting action, such as MnCl2 and SrCl2, and 5) AgNO3, which alone showed promoting action.
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PMID:Effects of metal elements on beta-hexosaminidase release from rat basophilic leukemia cells (RBL-2H3). 183 43

We report the cytotoxicity toward B16 cells and antitumor activity in three transplantable tumor models of a series of ionic, tetrahedral, bischelated gold diphosphine complexes of the type [Au1(R2PYPR2')2]X, where Y = (CH2)2, (CH2)3, or cis-CH = CH. The anion (X = Cl, Br, I, CH3SO3, NO3, PF6) had little effect upon activity. The R = R' = phenyl complexes 1, 7, and 8 [Y = (CH2)2, (CH2)3, cis-CH = CH, X = Cl] were the most active against P388 leukemia, with an increase in lifespan ranging from 83 to 92% and were also active against M5076 sarcoma and B16 melanoma. Complexes with pyridyl or fluorophenyl substituents had reduced activities. For the latter, 19F and 31P NMR were used to verify the formation of bischelated gold(I) complexes in solution. The reduced activity of the complex with R = Et and R' = Ph and inactivity with R = R' = Et are discussed in terms of their increased reactivity as reducing agents. 31P NMR studies show that [AuI(Et2P(CH2)2PPh2)2]Cl readily reacts with serum, albumin, and Cu2+ ions to give oxidized ligand.
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PMID:Cytotoxicity and antitumor activity of some tetrahedral bis(diphosphino)gold(I) chelates. 232 59

The antitumor and DNA-binding properties of a group of oligomeric platinum(II) and platinum(IV) complexes are described. The compounds, having the stoichiometry [cis-PtII(X)2(mu-OH)]2(NO3)2, where X is NH3, NH2CH2CH3, and NH2CH(CH3)2, were found to be inactive or only weakly active against L-1210 leukemia. In vitro studies involving PM2-DNA show that these compounds bind to and unwind closed circular DNA in a manner similar to cis-PtII-(NH3)2Cl2. The Pt(IV) complexes produced by hydrogen peroxide oxidation of the Pt(II) dimers are inactive as antitumor agents and are incapable of unwinding PM2-DNA. The cyclotrimer [cis-PtII(RR-DACH)(mu-OH)]3(NO3)3, where RR-DACH is (R,R)-1,2 diaminocyclohexane, exhibits potent antitumor activity against L-1210 leukemia and modest activities with B-16 and M5076 tumor lines. This compound platinates DNA, causing DNA unwinding and mobility shifts.
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PMID:Antitumor and DNA-binding properties of a group of oligomeric complexes of Pt(II) and Pt(IV). 237 44

The activity of nucleolar organizer regions (NOR) in chromosomes and interphase nuclei of bone marrow cells from 11 adult patients with acute lymphoblastic leukemia (ALL), 35 patients with acute nonlymphoblastic leukemia (ANLL), and eight healthy donors has been studied with silver nitrate staining. PHA-stimulated lymphocytes of the same individuals were used as standards of the maximum silver-staining patterns for each person. In 90% of patients with acute leukemia the average number of Ag+NOR in metaphases was lower when compared with that of PHA-stimulated lymphocytes. A variable expression of NOR was observed within the cell population and between individual patients. The populations tested showed high heterogeneity in relation to the content of Ag-negative mitoses. Ag+NOR per metaphase and the content of Ag-negative mitoses in bone marrow did not differ between patients with ALL and ANLL. Differences in the staining pattern in leukemic cells are discussed.
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PMID:The activity of nucleolar organizer regions of human bone marrow cells studied with silver staining. II. Acute leukemia. 243 24

Iron (Fe) depletion with anti-transferrin (Tf) receptor monoclonal antibodies (MAbs), Fe chelators, or gallium (Ga) salts inhibits in vitro and in vivo growth of tumor cells. The present studies examined the cytotoxic effects of an IgA anti-human Tf receptor MAb, 42/6, combined with parabactin, a powerful Fe chelator, or Ga nitrate. Parabactin inhibited in vitro growth of human hematopoietic and solid tumor cells, and the rank order of their sensitivities to the Fe chelator was identical to their relative sensitivity to MAb 42/6 as demonstrated in previous studies. When the most parabactin and MAb 42/6-sensitive (HL60 leukemia) and -resistant (KB carcinoma) cells were incubated with various concentrations of parabactin, cell killing was time and dose dependent over the first 24 hours. Little additional cytotoxicity occurred, however, when cells were exposed to parabactin for 48 hours. HL60 cells were slightly more sensitive than KB cells to parabactin cytotoxicity. Addition of optimally effective concentrations of anti-Tf receptor MAb 42/6 to parabactin increased cytotoxicity to HL60 cells over a narrow parabactin dose range but had little effect on cytotoxicity to KB cells. Cell cycle analysis of cells treated with parabactin for 24 hours showed that doses causing variable cytotoxicity increased the percentage of cells in S phase, but higher parabactin concentrations consistently arrested cells in G1 phase or at the G1/S interface. MAb 42/6 also increased toxicity of parabactin to granulocyte/macrophage colony-stimulating factors and normal marrow granulocyte/macrophage progenitors. When HL60 or KB cells were treated with MAb 42/6 combined with Ga nitrate, MAb 42/6 increased cytotoxicity of Ga for HL60 cells but had little or no effect on Ga cytotoxicity to KB cells. In contrast, MAb 42/6 had minimal effects on cytotoxicity of the ribonucleotide reductase inhibitor, isoquinaldehyde thiosemicarbazone, to either HL60 or KB cells. Both hematopoietic and solid tumors were killed by Fe depletion, but the present studies suggested that hematopoietic cells are more sensitive than solid tumor cells to cytotoxic effects of Fe depletion. Combined Fe depletion therapy by the use of MAb 42/6 with an Fe chelator or Ga salt increased toxicity to MAb 42/6-sensitive cells, such as HL60, but was not more effective against MAb 42/6-resistant solid tumor cells. Combination Fe depletion therapy of hematopoietic cell tumors merits evaluation in experimental in vivo tumor systems.
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PMID:Combination iron depletion therapy. 266 76

A series of 32 cationic platinum(II) complexes of the form cis-[PtA2(Am)Cl]+, where A is a monodentate (NH3 or i-PrNH2) or A2 is a bidentate (ethylenediamine or 1,2-diaminocyclohexane) amine and Am is either a heterocyclic amine based on a pyridine, pyrimidine, purine, piperidine, or a saturated amine (RNH2) ligand, was prepared and screened against in vivo murine tumor models. Each compound was tested against Sarcoma 180 ascites (S180a) in mice, with 20 members of the series showing activity (ILS greater than 50%). Antitumor activity also was demonstrated in 4 of 16 compounds tested in the L1210 murine leukemia model (ILS greater than 25%) and in 3 of 3 tested in the P388 murine leukemia model (ILS greater than 30%). The most active and potent analogues of the series were obtained when A was NH3 and Am was N1-pyridine, N1-4-methylpyridine, N1-4-bromopyridine, N1-4-chloropyridine, N3-cytosine, or N7-2'-deoxyguanosine. Complexes containing chelating and saturated amine ligands (A), as well as two trans isomers of active cis analogues (trans-[Pt(NH3)2(Am)Cl]+, where Am = N1-pyridine or N1-4-methylpyridine), were inactive in the S180a screen. All complexes were characterized by means of elemental analysis, HPLC, and 195Pt NMR spectroscopy, and the structure of one analogue, cis-[Pt(NH3)2(N3-cytosine)Cl](NO3), was determined by using single-crystal X-ray diffraction methods. While members of this series of compounds demonstrate antitumor activity in vivo, these new agents are not classical analogues of cisplatin (i.e. cis-[PtA2X2] complexes), as they contain three nitrogen donors and only one leaving group. The results of these studies suggest that further work should be conducted to better define the limits of the structure-activity relationships among platinum(II) complexes.
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PMID:Chemical and biological properties of a new series of cis-diammineplatinum(II) antitumor agents containing three nitrogen donors: cis-[Pt(NH3)2(N-donor)Cl]+. 290 24


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