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)

After completion of treatment with growth hormone (GH) 19 patients with isolated 'idiopathic' GH deficiency and 15 with post-irradiation GH deficiency underwent retesting of GH secretion with an insulin tolerance test or an arginine stimulation test, or both. Patients with post-irradiation GH deficiency comprised 13 patients with central nervous system tumours distant from the hypothalamo-pituitary axis and two with acute lymphoblastic leukaemia, who had received cranial or craniospinal irradiation. All 15 patients with post-irradiation GH deficiency remained GH deficient (peak GH response less than 7 mU/l (n = 10) and 7-15 mU/l (n = 5)). Of the 19 retested patients with idiopathic GH deficiency, however, five (26%) had peak GH responses of greater than 15 mU/l (regarded now as transient or false idiopathic GH deficiency) and were indistinguishable from the remainder (permanent or true idiopathic GH deficiency, peak GH responses less than 7 mU/l (n = 12) and 7-15 mU/l (n = 2)), by pretreatment anthropometry and post-treatment height standard deviation score, but had a lower first year height velocity (mean (SD) velocity 5.6 (0.5) cm/year for false idiopathic deficiency v 8.7 (1.75) cm/year for true idiopathic deficiency, p less than 0.01) and height increment on treatment (mean (SD) increment 2.2 (1.5) cm/year for false idiopathic deficiency v 5.2 (2.3) cm/year for true idiopathic deficiency, p less than 0.05). By current practices two patients with false idiopathic deficiency may have been distinguished by sex steroid priming. Thus post-irradiation GH deficiency seems to be permanent, but errors in diagnosis in idiopathic GH deficiency are common.
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PMID:Growth hormone state after completion of treatment with growth hormone. 356 14

Five male children who received cranial irradiation for extrahypothalamic intracranial neoplasms or leukemia and subsequently developed severe growth hormone (GH) deficiency were challenged with synthetic growth hormone-releasing factor (GRF-44), in an attempt to distinguish hypothalamic from pituitary dysfunction as a cause of their GH deficiency, and to assess the readily releasable GH reserve in the pituitary. In response to a pulse of GRF-44 (5 micrograms/kg intravenously), mean peak GH levels rose to values higher than those evoked by the pharmacologic agents L-dopa or arginine (6.4 +/- 1.3 ng/mL v 1.5 +/- 0.4 ng/mL, P less than .05). The peak GH value occurred at a mean of 26.0 minutes after administration of GRF-44. These responses were similar to those obtained in children with severe GH deficiency due to other etiologies (peak GH 6.3 +/- 1.7 ng/mL, mean 28.0 minutes). In addition, there was a trend toward an inverse relationship between peak GH response to GRF-44 and the postirradiation interval. Prolactin and somatomedin-C levels did not change significantly after the administration of a single dose of GRF-44. The results of this study support the hypothesis that cranial irradiation in children can lead to hypothalamic GRF deficiency secondary to radiation injury of hypothalamic GRF-secreting neurons. This study also lends support to the potential therapeutic usefulness of GRF-44 or an analog for GH deficiency secondary to cranial irradiation.
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PMID:Effect of growth hormone-releasing factor on growth hormone release in children with radiation-induced growth hormone deficiency. 392 54

N-terminal amino acid sequence analysis of the transmembrane protein of baboon endogenous virus revealed an internal 13 residue identity with the transmembrane homolog of murine leukemia virus. A tridecapeptide Glu-Val-Val-Leu-Gln-Asn-Arg-Arg-Gly-Leu-Asp-Leu-Leu corresponding to this region was chemically synthesized and antibody to the peptide was raised in rabbits. The rabbit antisera recognized the protein in Western blots. The specificity of the antisera was tested against a panel of retroviruses. Transmembrane proteins of type C retroviruses as well as type D were identified.
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PMID:Antibody to a synthetic peptide detects a conserved region of retrovirus transmembrane proteins. 397 84

The effect of lysine/arginine antagonism on the survival of mice with virally - produced leukemia was investigated by feeding AKR mice diets low in arginine with varying amounts of lysine. Over a period of one year, a diet containing 5.6% lysine and no arginine resulted in a significantly lower mortality than one with lower levels of lysine, plus arginine.
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PMID:Effect of lysine on survival of AKR leukemic mice. 609 57

The effect of cranial irradiation with doses of 2,400 and 4,800 rad on the pituitary function of children with acute lymphoblastic leukaemia was studied. The plasma growth hormone level after arginine simulations was normal in 13 out of 15 children. The rise of TSH after TRH stimulation and the metyrapone test were also normal. The growth of 40 children during an observation period of 3 or more years was also normal.
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PMID:[Pituitary function and growth in children under treatment for leukemia (author's transl)]. 610 41

The viral proteins of Moloney murine sarcoma virus-transformed mouse cells (G8-124), that overproduce the sarcoma virus relative to helper leukemia virus, were examined by immunoprecipitation, sizing by gel electrophoresis and peptide mapping. Using antisera to the viral core proteins, a p10-deficient core polyprotein of 63 000 daltons (P63gag) was detected which was found to be a product of the MuSV-124 genome. Helper virus proteins Pr67gag, gPr85gag, Pr200gag-pol, and gPr83env were also detected and characterized. An unusual helper virus precursor polyprotein of 93 000 daltons was also detected and characterized. It was labeled with [3H]fucose, suggesting that it was an intermediate precursor containing gp70 on which further modification of the core oligosaccharide had occurred relative to gPr83env. The usual viral proteins were also found in sarcoma virus particles and they were undistinguishable in size from those of Moloney murine leukemia virus (cl-1 strain). These experiments together with pulse-labeling experiments performed in the presence of the arginine analog canavanine, which prevents proteolytic cleavage, suggest that the product derived from the Mo-MuSV-specific sequences must be expressed as a separate gene product since we were unable to detect in transformed cells a polyprotein containing both viral (e.g., 'gag', 'pol' or 'env') and non-viral components. Cell-free protein synthesis studies performed with Mo-MuSV-124 genomic RNA have confirmed this interpretation and have identified three size classes of polypeptides as translation products of the sarcoma virus genome. They are P63gag, P42-P38 and P23. Intracellular p63gag and cell-free synthesized P63gag, appear to have identical sizes, antigenic determinants and tryptic peptides. The P42-P38 proteins contain core protein determinants. P23 is not related to the products of the replication genes of MuLV. Thus, P23 is a candidate for the 'src' gene product of Mo-MuSV-124.
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PMID:Characterization of viral polyproteins in cells transformed and producing Moloney murine sarcoma virus-124. 615 3

1. Substance P (SP) induces histamine release from isolated rat peritoneal mast cells at concentrations of 0.1-10 muM.2. Inhibitors of glycolysis and oxidative phosphorylation prevent the release of histamine induced by SP.3. Cells heated to 47 degrees C for 20 min release histamine when treated with an agent causing cell lysis but fail to release in response to SP.4. SP does not release histamine by interacting with cell-bound IgE.5. Histamine release by SP is rapid, with more than 90% of the response occurring within 1 min of the addition of the peptide to mast cells at 37 degrees C.6. Substance P, unlike antigen-antibody or compound 48/80, does not show enhanced release of histamine when calcium (0.1-1 mM) is present in the extracellular medium but calcium increases the response to SP when the ion is added after the peptide. Extracellular calcium (0.1-1 mM), magnesium (1-10 mM) and cobalt (0.01-0.1 mM) all inhibit SP-induced histamine release when added before the peptide. Pre-treatment of the cells with EDTA (10 mM) and washing in calcium-free medium inhibits the histamine release induced by SP.7. Histamine release induced by SP was optimum at an extracellular pH of 7.2.8. A number of peptides structurally related to SP were examined for histamine-releasing activity. At the concentrations tested, the N-terminal dipeptides Lys-Pro and Arg-Pro, tuftsin, physalaemin, eledoisin, SP(3-11), SP(4-11) and [p-Glu(6), p-amino Phe(7)]-SP(6-11) were all found to be inactive. The relative activities of the other peptides were: [Formula: see text]9. Rat basophilic leukaemia cells (RBL-2H3) fail to respond to SP at concentrations which activate rat mast cells. Release of 5-hydroxytryptamine by immunological activation of RBL cells is not changed by the presence of SP.10. The mechanism of action of SP on mast cells and the nature of the SP receptor on mast cells is discussed in relation to SP receptors in other cell types.
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PMID:The effects of substance P on histamine and 5-hydroxytryptamine release in the rat. 618 68

AKR mice, known to develop spontaneous leukemia in almost 100% of cases, were studied throughout their life-span. Different treatments combining a potent immune stimulator, Corynebacterium parvum (CP), with interferon (IFN) and arginine butyrate were initiated at the 15th week of life. In a preliminary series of experiments, CP (200 micrograms), IFN (20,000 units) and butyrate 50 mM) were employed in a well-defined chronological order. In controls, the mean survival time (MST) was 35.17 +/- 1.67 weeks and the final survival rates was 0/50 mice for all experiments. Only CP associated with arginine butyrate significantly augmented the MST (42.5 +/- 3.66 weeks) and final survival rate (9/35 mice). In an adjusted set of experiments, reducing the IFN concentration to 10,000 and 5,000 units and that of butyrate to 6 mM greatly improved the results. The MST was substantially increased with the combinations of CP + IFN + butyrate (41.4 +/- 1.86 weeks), CP + IFN (42.73 +/- 3.29 weeks) and butyrate + IFN (41 +/- 2.34 weeks), as well as the final survival rates (8/15, 10/15 and 6/15 mice respectively). An important finding was that when CP and IFN were used separately, they were ineffective.
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PMID:Effect of coordinated therapeutic assays using C. parvum, interferon and arginine butyrate on spontaneous disease and survival of AKR mice. 619 71

Two proteins, termed gp60 and p30, have been purified to homogeneity from bovine leukemia virus (BLV) using controlled pore glass and reverse-phase liquid chromatography (RPLC). gp60 was shown to be a glycoprotein by identification of glucosamine on the amino acid analyzer. Antiserum prepared to gp60 recognized in addition to gp60 a 52,000-Da polypeptide in some virus preparations, but did not cross-react with p30. The amino and carboxyl termini of gp60 were found to be tryptophan and arginine, respectively, and a 38-residue amino-terminal sequence of gp60 (NH2TrpArgXSerLeuSerLeuGlyAsnGlnGlnTrpMetThrAlaTyrAsnGlnGluAlaLys PheSerIleSerIleAspGlnIleLeuGluAlaHisAsnGlnSerProPhe-) was obtained. A 12-residue amino-terminal sequence for p30 (NH2SerProValAlaAlaLeuThrLeuGlySerAlaLeu) was also obtained. The p30 sequence showed substantial homology to the transmembrane proteins of both types B and C retroviruses and also to a deduced sequence of the 3' region of the env gene of human T-cell leukemia virus. From these results and from elution behavior of these proteins on RPLC, it was concluded that gp60 and p30 are the BLV env gene-encoded surface glycoprotein and transmembrane protein, respectively.
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PMID:The envelope proteins of bovine leukemia virus: purification and sequence analysis. 620 44

We have used site-directed mutagenesis of cloned Moloney murine leukemia virus (MuLV) DNA to define a function encoded in the 3' region of the viral pol gene and required for efficient integration of viral DNA. One mutant, MuLV-SF1, contained a single base substitution (C to T at base 4950) that resulted in an arginine to cysteine change in a region highly conserved among retroviruses. Mutant DNA, introduced into rat cells by cotransfection with a herpes simplex virus thymidine kinase gene (HSV tk), directed production of virus particles with reverse transcriptase activity. Infection of cells with these particles led to synthesis of full-length linear and circular forms of unintegrated viral DNA; however, integrated viral DNA was decreased at least by a factor of 10 when examined by DNA hybridization, and the mutant particles were less efficient then wild-type virus at establishing an infection by a factor of at least 300. Pseudotypes formed with the proteins of MuLV-SF1 and the genome of a replication defective marker MuLV, carrying the HSV tk gene, were less effective by at least a factor of 100 in producing tk+ colonies than pseudotypes formed with proteins encoded by wild-type virus. When the MuLV-SF1 pseudotypes did produce tk+ cells, most of the proviruses were integrated aberrantly. We conclude that the MuLV-SF1 pol gene is defective for a function that is required for normal integrative recombination and dissociable from DNA synthesis.
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PMID:A mutant murine leukemia virus with a single missense codon in pol is defective in a function affecting integration. 620 50


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