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)

Neither indomethacin nor aspirin, at concentrations which inhibited the formation of prostaglandins and prevented the interferon-induced increase in the intracellular concentration of cyclic GMP, had any significant effect on the development of the interferon-induced antiviral state either in mouse L1210 cells challenged with vesicular stomatitis virus or in mice infected with encephalomyocarditis virus. Furthermore, neither drug had any significant effect on the interferon-induced inhibition of cell multiplication in cultures of mouse leukaemia L1210 cells. The differences in the effects of these cyclo-oxygenase inhibitors on different interferon effects may provide some insight into the different pathways of interferon action.
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PMID:Indomethacin and aspirin do not inhibit the antiviral or anti-proliferative actions of interferon. 618 29

The effects of cyclic nucleotides and PGE1 upon the proliferation of normal granulocyte/macrophage progenitors were examined in in vitro systems and contrasted to the effects of these compounds on (1) granulocyte/macrophage progenitors from the peripheral blood of patients with myeolofibrosis/myeloid metaplasia (MF) and chronic myelogeneous leukemia (CML); and (2) blast progenitors from the peripheral blood of patients with acute myelogenous leukemia (AML) and acute monocytic leukemia (AMoL). Cyclic AMP was found to be a concentration dependent inhibitor of colony proliferation in all systems tested. Cyclic GMP was an inconsistent enhancer of colony proliferation in all systems in a manner which was not clearly concentration dependent. The effect of PGE1 in normal systems was highly variable depending on the culture conditions, but it was generally found to be an inhibitor of colony proliferation. Cyclic AMP, cyclic GMP and PGE1 altered the release of colony stimulating activity from adherent bone marrow cells in a manner opposite to the direct effects of these compounds on progenitor cell proliferation. Abnormalities in response to PGE1 were found in progenitors from patients with CML (deficient inhibition), AMoL (stimulation of proliferation in certain concentration ranges), and MF (enhanced proliferation). Studies on one of the patients with MF indicated that a normally responding population could be defined by density-gradient separation. These data confirm the capacity of these compounds to modulate in vitro proliferation of myeloid progenitors, and suggest that aberrations of response to PGE1 may occur in subpopulations of cells from several myeloproliferative disorders.
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PMID:Modulation of normal and abnormal myeloid progenitor proliferation by cyclic nucleotides and PGE1. 625 72

Cyclic cytidine 3':5'-monophosphate (cyclic CMP), cyclic guanosine 3':5'-monophosphate (cyclic GMP), and cyclic adenosine 3':5'-monophosphate (cyclic AMP) contents of leukocytes and urines of leukemic patients have been investigated. We have studied four types of leukemia: acute myeloblastic leukemia; chronic myelocytic leukemia; acute lymphoblastic leukemia; and chronic lymphocytic leukemia. As controls, the cyclic nucleotide content of leukocytes and urines of healthy volunteers and patients with solid tumors selected for their normal hemogram has been determined. It has also been measured in phytohemagglutinin-stimulated lymphocytes. Our data show that: (a) the concentration of cyclic CMP is always lower than that of cyclic GMP or cyclic AMP; (b) in urines, the concentrations of the three nucleotides are higher in patients than in healthy volunteers, the greatest differences being observed between the cyclic CMP concentrations of acute leukemia patients and controls; and (c) in white blood cells, cyclic AMP concentration is lower in leukemic than in normal cells. The cyclic GMP concentration is the same everywhere except in monoblastic cells and leukocytes from solid tumor patients. High cyclic CMP levels are associated only with acute leukemia, whether myeloblastic, monoblastic, or lymphoblastic, a fact which suggests that cyclic CMP could be a biochemical marker of hematopoietic stem cell malignancy.
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PMID:Relationship between the levels of cyclic cytidine 3':5'-monophosphate, cyclic guanosine 3':5'-monophosphate, and cyclic adenosine 3':5'-monophosphate in urines and leukocytes and the type of human leukemias. 626 79

Plasma and urine levels of cyclic adenosine 3',5'-monophosphate (cAMP) and of cyclic guanosine 3',5'-monophosphate (cGMP) were measured in 35 normal subjects, in 24 patients with nonneoplastic diseases (iron deficiency anemia, peptic ulcer, and cholelithiasis), and in 50 leukemic patients. The leukemic group included patients with acute lymphoblastic leukemia, acute myelogenous leukemia, chronic lymphocytic leukemia, and chronic myelogenous leukemia. All patients were recently diagnosed and untreated, except for 5 patients with blastic transformation of chronic myelogenous leukemia who had been previously treated. There were no significant differences in plasma and urine cyclic nucleotide levels between normal subjects and patients with nonneoplastic diseases. In leukemic patients, plasma and urine cAMP levels were similar to those of normal subjects, whereas plasma and urine cGMP levels were markedly elevated. There were no significant differences in cGMP values between the various types of leukemia. After starting treatment, plasma cyclic nucleotide levels were periodically measured in 21 of the patients with acute leukemia; cGMP levels were normalized in all the 16 subjects who attained complete remission, whereas both cAMP and cGMP levels were apparently unaffected in the patients who did not respond to treatment. This suggests that plasma or urine cGMP could be used as an additional parameter to monitor the patient's response to treatment.
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PMID:Plasma and urine cyclic nucleotide levels in patients with acute and chronic leukemia. 629 36

The effect of Escherichia coli heat-stable (ST) enterotoxin on calcium and cyclic nucleotide metabolism in rat basophilic leukemia cell cultures was investigated. Addition of ST enterotoxin to rat basophilic leukemia cell cultures resulted in dose- and time-dependent stimulation of calcium uptake and elevation of the intracellular cyclic GMP (cGMP) concentration. The effect of ST enterotoxin on calcium uptake (P less than 0.02) and cGMP synthesis (P less than 0.02) was demonstrated after 5 and 30 min of incubation at 37 degrees C, respectively. In further studies ST enterotoxin did not enhance calcium release or the intracellular concentration of cyclic AMP. The stimulation of calcium uptake and cGMP synthesis by ST enterotoxin was inhibited by pharmacological and chemical agents which block cellular calcium entry and prostaglandin synthesis. These results demonstrate that ST enterotoxin induces calcium uptake and cGMP synthesis in rat basophilic leukemia cell cultures.
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PMID:Stimulation of calcium uptake and cyclic GMP synthesis in rat basophilic leukemia cells by Escherichia coli heat-stable enterotoxin. 630 75

Plasma levels of cyclic AMP and cyclic GMP were determined in 35 guinea pigs for up to 9 days following subcutaneous passage of L2C leukemia cells. Twenty guinea pigs into which normal syngeneic guinea pig thymocytes were passaged served as controls. Cyclic AMP levels in plasma showed little change and were only elevated significantly in test animals on day 9 after passage. In contrast cyclic GMP levels reached a maximum on day 5 after passage of leukemia cells with two to threefold rises over day 1 levels. Increases in leukocyte counts were not observed until day 7 in test animals. Of the other tumour growth indices which were examined, the axillary (draining) node index gave the earliest indication of cell proliferation, with significant elevations on day 3 after passage. The authors conclude that plasma cyclic GMP increases precede increases in white cell counts by at least 2 days, and may reflect an early increase in axillary node growth.
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PMID:Changes in guinea pig plasma cyclic nucleotide levels during the development of a transplantable leukemia. 631 60

Cholera enterotoxin (CT), at an optimal concentration of 2.38 X 10(-10) M, stimulated calcium uptake (P less than 0.01) and cyclic AMP accumulation (P less than 0.02) in cultured rat basophilic leukemia cells. No significant effect of CT on calcium release or cyclic GMP accumulation was detected. Pharmacologic and chemical agents which block calcium uptake or prostaglandin synthesis antagonized the effect of CT.
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PMID:Effect of cholera enterotoxin on calcium uptake and cyclic AMP accumulation in rat basophilic leukemia cells. 632 Dec 61

Many antidepressants inhibit 5-hydroxytryptamine (5HT) transport resulting in increased 5HT levels in the synapse. However, physiological regulation of neurotransmitter uptake has not been demonstrated. We have examined the effect of receptor-activated second messengers on the 5HT transporter in rat basophilic leukemia cells (RBL 2H3). Here, we show that activation of an A3 adenosine receptor results in an increase of 5HT uptake in RBL cells, due to an increase in maximum velocity (Vmax). The A3 adenosine receptor-stimulated increase in transport is blocked by inhibitors of nitric oxide synthase and by a cGMP-dependent kinase inhibitor. In fact, compounds that generate nitric oxide (NO) and the cGMP analog 8-bromo-cGMP mimicked the effect of A3 receptor stimulation, suggesting that the elevation in transport occurs through the generation of the gaseous second messenger NO and a subsequent elevation in cGMP. Additionally, the 5HT transporter is differentially regulated by second messengers since direct activation of protein kinase C by phorbol esters decreases 5HT uptake by decreasing Vmax. Our results suggest that the changes in transport are due to a direct modification of the 5HT transporter, possibly by phosphorylation, which appears to alter the rate at which transport occurs. As the 5HT transporter in RBL cells is identical to that in neurons, our results suggest that analogous mechanisms may operate in the brain.
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PMID:Adenosine A3 receptors regulate serotonin transport via nitric oxide and cGMP. 752 54

A subclone of the EoL-3 human eosinophilic leukemia cell line (EoL-3.12) was selected for its high inducibility of CD23 (low affinity IgE receptor/Fc epsilon RII) by IL-4. Maximum membrane CD23 expression was detected after 16 h of incubation with IL-4, then gradually returned to basal level after 48 h. Membrane expression of CD23 on EoL-3.12 cells was found to parallel their homotypic aggregation. Extending the time of incubation with IL-4 to 48 h or more resulted in a de-aggregation of cells of cells with a shedding of membrane CD23 and an increase of its soluble form, sCD23. The IL-4-induced aggregation of EoL-3.12 cells was inhibited with anti-CD23 antibody or human myeloma IgE protein, indicating that it was mediated through the engagement of CD23. EoL3.12 incubated with IL-4 displayed morphological changes associated with differentiation, such as an increased number of lobulated nuclei with prominent nucleoli, increased ratio of cytoplasm and distinct cytoplasmic processes. EoL-3.12 cells incubated with IL-4 also displayed an enhanced adherence to human umbilical vein endothelial cells (HUVEC), which was reverted when the IL-4 incubation time extended. Furthermore, the transendothelial migration of EoL-3.12 cells toward a chemokinetic gradient of soluble CD23 (sCD23; 29 kDa fragment) closely paralleled the density of membrane CD23 expressed on EoL-3.12 cells. Additionally, the engagement of CD23 led to the activation of the L-arginine-dependent pathway of nitric oxide (NO) production, as detected by the increase in intracytoplasmic cGMP concentration. The capacity of EoL-3.12 cells to form homotypic as well as heterotypic adhesion appears therefore to be regulated, at least in part, by the level of CD23 expression.
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PMID:Involvement of CD23/Fc epsilon RII in the homotypic and heterotypic cytoadhesion of the human eosinophilic cell line Eol-3. 858 71

Whole-cell patch clamp experiments were performed to examine the effects of the nonhydrolyzable GTP analogue, guanosine 5'-3-O-(thio)triphosphate, on membrane currents in rat basophilic leukemia cells. Guanosine 5'-3-O-(thio)triphosphate activated an inward sodium current. This current had a new permeability sequence to monovalent cations and a different pharmacological profile to that of other characterized Na+ channels. Long hyperpolarizing steps revealed that the current declined during the pulse, and the decline was voltage-dependent. Activation of the current required Mg2+ and ATP. The nonhydrolyzable ATP analogues, adenosine 5'-O-(thio)triphosphate and adenosine 5'-(beta,gamma-imino)triphosphate, could not substitute for ATP. Soluble second messengers like cAMP, cGMP, inositol polyphosphates, and Ca2+ did not activate the Na+ current. These results suggest that nonhydrolyzable GTP analogues activate a Na+ current in rat basophilic leukemia cells that is new in terms of its selectivity, pharmacology, and activation mechanism. It may be the prototype for a new family of Na+ channels expressed in certain nonexcitable cells.
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PMID:Nonhydrolyzable analogues of GTP activate a new Na+ current in a rat mast cell line. 879 10


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