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)

Phosphotyrosine-containing proteins were detected by western blotting of whole cell lysates of purified human neutrophils or rat basophilic leukemia cells (RBL-2H3) using a polyclonal anti-phosphotyrosine antibody. When either cell type was stimulated with the appropriate Fc crosslinking agent, heat-aggregated IgG for the neutrophil or DNP-HSA for the IgE-sensitized RBL-2H3, a rapid increase in the phosphotyrosine content of several proteins was observed. The kinetics and specificity of both responses suggest that Fc receptor crosslinking activates a receptor-associated tyrosine kinase, probably a member of the src family of tyrosine protein kinases. The subsequent tyrosine phosphorylation events are likely to be important in Fc receptor-mediated stimulus-response coupling in inflammatory cells.
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PMID:Tyrosine phosphorylation is an early signaling event common to Fc receptor crosslinking in human neutrophils and rat basophilic leukemia cells (RBL-2H3). 171 Apr 46

Homologs to genes residing on human chromosome 3 (HSA 3) map to four mouse chromosomes (MMU) 3, 6, 9, and 16. In the bovine, two syntenic groups that contain HSA 3 homologs, unassigned syntenic groups 10 (U10) and 12 (U12), have been defined. U10 also contains HSA 21 genes, which is similar to the situation seen on MMU 16, whereas U12 apparently contains only HSA 3 homologs. The syntenic arrangement of other HSA 3 homologs in the bovine was investigated by physically mapping five genes through segregation analysis of a bovine-hamster hybrid somatic cell panel. The genes mapped include Friend-murine leukemia virus integration site 3 homolog (FIM3; HSA 3/MMU 3), sucrase-isomaltase (SI) and glutathione peroxidase 1 (GPX1) (HSA 3/MMU ?), murine leukemia viral (v-raf-1) oncogene homolog 1 (RAF1; HSA 3/MMU 6), and ceruloplasmin (CP; HSA 3/MMU 9). FIM3, SI, and CP mapped to bovine syntenic group U10, while RAF1 and GPX1 mapped to U12.
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PMID:Mapping HSA 3 loci in cattle: additional support for the ancestral synteny of HSA 3 and 21. 178 81

The specificity of the p15 proteinase of myeloblastosis-associated virus (MAV) was tested with nonviral high molecular weight substrates and with synthetic peptides. Peptides with sequences spanning known cleavage sites in viral polyproteins of Rous sarcoma virus (RSV) and avian leukemia viruses, as well as in BSA and HSA, were synthesized, and the rate of their cleavage by the MAV proteinase was compared. Synthetic peptides require for successful cleavage at least 4 residues at the N-terminal side and 3 residues at the C-terminal side. The proteinase shows a preference for hydrophobic residues with bulky side chains (Met, Tyr, Phe) in P3, although Arg and Gln can also be accepted. Small hydrophobic residues are required in P2 and P2', and large hydrophobic residues (Tyr, Met, Phe/p-nitro-Phe) are preferred in both P1 and P1'. The difference between the specificity of the p15 proteinase and that of the HIV-1 proteinase mostly pertains to position P2' of the substrate, where bulkier side chains are accepted by the HIV-1 proteinase (Richards et al., 1990). A good chromogenic substrate for the MAV and RSV proteinases was developed and used to further characterize the MAV proteinase activity with respect to ionic strength and pH. The activity of the proteinase is strongly dependent on ionic strength and pH. Both the kcat and Km values contribute to a higher cleavage efficiency at higher salt concentrations and show a bell-shaped pH dependence curve with a sharp maximum at pH 5.5 (kcat) and 6.5 (Km).
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PMID:Specificity studies on retroviral proteinase from myeloblastosis-associated virus. 184 25

We have previously shown that, unlike monomeric IgE, chemically derived dimers, trimers, and heavier oligomers of IgE were internalized efficiently. This finding suggested that endocytosis, like mediator release, is triggered by cross-linking of the cell surface receptors for IgE. In the present study, we analyzed the temporal and functional relationships between the two events. We used rat basophilic leukemia cells (RBL-HR+-2H3) and rat peritoneal mast cells, which were allowed to bind monomeric 125I mouse IgE hybridoma anti-dinitrophenyl (HI-DNP-E-26-82), and the polyvalent antigen 131I-dinitrophenylated human serum albumin (DNP15-HSA). We found that at 37 degrees C, 50% of the cell surface-bound immune complexes were internalized rapidly (t1/2 3 to 5 min) by RBL-HR+-2H3 cells with only minimal reduction (1/3) in the extent of internalization when very few of the receptors (approximately 5%) were saturated with IgE. Normal mast cells internalized cell surface-bound immune complexes at a similar rate (t1/2 4 to 5 min). Unlike serotonin release, internalization was independent of extracellular calcium and continued to increase as the ratio of DNP15-HSA to IgE increased 10- to 100-fold over the ratio required for optimal histamine release. In the RBL cells, internalization preceded serotonin release, reaching a peak at about 10 min, while the release (t1/2 13 to 19 min) continued for up to 60 min. Presumably, some of the cross-linked IgE internalized less effectively and continued to trigger serotonin release. The reverse relationship between the rates of internalization and release (t1/2 less than 1 min) was found in normal rat mast cells. We conclude that although cross-linking of two or more receptors triggered both endocytosis and exocytosis, the two events are not necessarily sequential.
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PMID:The fate of IgE bound to rat basophilic leukemia cells. III. Relationship between antigen-induced endocytosis and serotonin release. 620 83

The application of recombinant DNA technologies has allowed the detection of at least three families of moderately repetitive DNA segments in the human genome that are homologous to retroviruses previously isolated from mice and primates. One of these DNA segments has been shown by nucleotide sequence comparisons to be distantly related to both Moloney murine leukaemia virus (MoMuLV) and the endogenous baboon retrovirus and to have the sequence organization characteristic of an integrated retrovirus. Isolation of the homologous locus from chimpanzee DNA indicated that the integration event preceded the evolutionary divergence of chimpanzees and man. Here we have used a panel of rodent x human somatic cell hybrids to assign the chromosomal localization of this segment, called ERV1 (endogenous retrovirus-1), to human chromosome 18 (HSA 18).
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PMID:Mapping of an endogenous retroviral sequence to human chromosome 18. 684 62

Human macrophage colony-stimulating factor (hM-CSF) is a potent stimulator of the effector functions of monocytes/macrophages. We investigated the antitumor effects of this factor in CDF1 male mice inoculated with L1210 cells, a mouse B-cell leukemia line. Mice preinoculated with various numbers of L1210 cells on day 0 were given intravenous injections of vehicle (human serum albumin; HSA) (100 micrograms/kg/day) or hM-CSF (20 micrograms/kg/day) for 3 days from day 1. In mice preinoculated with 10(2) L1210 cells but not with 10(3) or more L1210 cells, a marked increment in survival rate was observed with hM-CSF treatment. We next examined the effect of hM-CSF treatment combined with chemotherapy on the survival of mice that had been preinoculated with 10(5) L1210 cells. In our system, the administration of 4.9 mg/kg adriamycin (ADM) alone slightly prolonged survival of the tumor-bearing mice, but all of the mice died within 20 days. When hM-CSF was injected for 3 days before this ADM treatment, the invasion and proliferation of tumor cells in the liver and spleen were markedly inhibited and 50% of the mice were still alive at day 50. We detected inhibitory activity toward L1210 growth in serum of mice administered with hM-CSF, and the degree of the inhibitory activity was correlated with the level of nitrite (NO2-) in the serum. When L1210 cells were co-cultured with peritoneal macrophages from mice intraperitoneally injected with hM-CSF, the uptake of [3H]thymidine in L1210 cells was inhibited. The inhibition was abolished by the addition of NG-monomethyl-L-arginine, an inhibitor of NO2- synthesis, suggesting that the reactive nitrogen oxide intermediate is involved in hM-CSF-induced inhibition of L1210 growth.
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PMID:Augmentation of cancer chemotherapy by preinjection of human macrophage colony-stimulating factor in L1210 leukemic cell-inoculated mice. 753 4

Rat basophil leukemia (RBL) cells were sensitised with varying proportions of monoclonal IgE anti-ovalbumin (OVA) and anti-DNP antibodies, and serotonin release was measured after challenge with aggregated OVA or dinitrophenylated human serum albumin (DNP-HSA). Highly aggregated OVA was shown to provoke the degranulation of RBL cells that had been sensitised with an IgE preparation containing 2% IgE anti-OVA antibodies. Highly substituted DNP32-HSA induced degranulation of RBL cells sensitised with just 0.5% antigen-specific IgE. When cells were sensitised with high percentages of specific IgE, maximum degranulation was seen at concentrations of 2 micrograms/ml (aggregated OVA) and 50 ng/ml (DNP-HSA), while moderate degranulation was still seen at antigen concentrations as low as 50 and 2 ng/ml, respectively. Low-molecular weight aggregates of OVA and low-valency DNP4-HSA only stimulated degranulation when high percentages of RBL Fc epsilon receptor were occupied by antigen-specific IgE. The sensitising abilities of two anti-DNP monoclonal antibodies of differing affinities were compared. When challenged with low-valency antigen, only cells sensitised with the higher-affinity monoclonal antibody exhibited moderate levels of degranulation. Degranulation required exposure to high antigen challenge doses (5 micrograms/ml). Cells sensitised with either monoclonal antibody responded strongly when challenged with a wide range of concentrations (1-250 ng/ml) of high-valency DNP32-HSA, although greater sensitivity was always seen with the higher-affinity antibody. These results suggest that antigen valency is a critical parameter for mast cell function, and that low-affinity antibody may be capable of sensitising mast cells to high-valency antigen.
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PMID:Antigen valency as a determinant of the responsiveness of IgE-sensitised rat basophil leukemia cells. 762 Mar 69

v-mpl is a constitutively activated, truncated form of a cytokine receptor that has been transduced in a murine retrovirus, the myeloproliferative leukemia virus (MPLV). Expression of this oncogene results in the factor-independent proliferation of myeloid, erythroid, megakaryocytic, and mast precursor cells, which retain the ability to differentiate. However, no lymphoid disease was ever reported. To determine whether MPLV could infect and transform very early B cells and their precursors (BCPs), lymphoid long-term bone marrow cultures were infected with a helper-free MPLV. Within 3 wk after infection, highly proliferating BCPs could be isolated. These cells were able to clone spontaneously in semi-solid cultures, grown in the absence of feeder cell layer or exogenous growth factor and rapidly produced tumors after s.c. injection into synegic irradiated mice. In addition, MPLV transformation of pre-B cells led to the induction of an autocrine activity. Immunophenotypic and molecular analysis indicated that MPLV transformed early pro-B, pro-B, and pre-B cells, according to the expression of HSA, CD43, B220, Thy1, s-IgM and BP1 Ags, and to the rearrangements of Ig genes. Interestingly, MPLV-transformed BCPs expressed Mac1 Ag without acquiring further characteristics of macrophagic differentiation. Although the v-mpl cytoplasmic domain is devoid of tyrosine kinase consensus sequence, MPLV-transformed pre-B cells contained a major approximately 105-kDa tyrosine-phosphorylated protein that was not detected in uninfected cells or in cells transformed by the Abelson viral oncogene (v-abl). These results demonstrate that, like v-abl, the truncated cytokine receptor v-mpl is able to transform BCPs in vitro and suggest that the oncogenic transformation of BCPs by either v-mpl or v-abl use different pathways.
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PMID:In vitro transformation of murine pro-B and pre-B cells by v-mpl, a truncated form of a cytokine receptor. 783 43

In order to elucidate the involvement of adhesion mechanisms in the process of megakaryocyte-dependent fibroblast growth, we applied BSA-coupled polymers of glucose, galactose, fucose, mannose, and several lectins (AAA, LCA, LTA, UEA-I) to cocultures of CD61 -positive (CD61+)/MACS-enriched megakaryocytes and human bone marrow fibroblasts. Fibroblast monocultures served as controls. After 6 days, glucose, as well as galactose-treated cultures showed a significant reduction of fibroblast growth in cocultures and fibroblast monocultures. In contrast, application of mannose caused no reducing effect on fibroblast numbers. Administration of fucose, AAA, LTA or UEA-I revealed a strong impairment of fibroblast growth in the megakaryocyte-fibroblast cocultures. Adhesion experiments using MACS-enriched, fluorescein-labelled megakaryocytes cultured in the presence of carbohydrates and lectins on a near-confluent layer of fibroblasts were additionally performed. Following fucose-BSA, alpha Fuc-1,2Gal beta-HSA or UEA-I treatment a significant reduction of megakaryocyte adhesion to the fibroblast layer could be observed. In the case of AAA a weak impairment of megakaryocyte adhesion could be noticed. Selective pretreatment of either fibroblasts or megakaryocytes with fucose-BSA or alpha Fuc-1,2Gal beta-HSA was consistent with the finding of a prominent involvement of fucosylated residues located on megakaryocytes in this interaction. In conclusion, our studies are in keeping with the assumption that fucosylated and fucose-binding structures are playing a key role in adhesion mechanisms between megakaryocytes and fibroblasts and thus influence significantly the megakaryocyte-dependent growth of bone marrow fibroblasts.
Leukemia 1996 Oct
PMID:Interactions between endogeneous lectins and fucosylated oligosaccharides in megakaryocyte-dependent fibroblast growth of the normal bone marrow. 884 95

A primer pair, PB and BSH, which amplified alts, a portion of Candida albicans-specific repetitive sequence, RPS, gave stable and reproducible fingerprint patterns of the strains by polymerase chain reaction (PCR). We applied this method to clinical isolates of C. albicans for strain discrimination. Using PCR fingerprint patterns, we could analyze the relatedness of C. albicans strains including those isolated from children with leukemia and their bedside parents. The results indicated that PCR analysis targeting an alt region gives rise to the same conclusion as the previous study obtained by SmaI RFLP analysis.
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PMID:Discrimination among the clinical isolates of Candida albicans by amplification of the repetitive sequences, alts. 957 Feb 88


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