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)

WE REEXAMINED TWO QUESTIONS CONCERNING LYT ANTIGENS OF CYTOTOXIC T CELLS OF THE MOUSE: is Lyt-1 antigen expressed on cytotoxic effector cells and can cytotoxicity be blocked by antibody to Lyt antigens in the absence of added complement? A 3-hr (51)Cr-release assay with splenic effector cells and leukemia or myeloma target cells was used to measure cell-mediated cytotoxicity. The cytotoxic activity of effector cells against allogeneic targets was abolished by exposure to Lyt-1, Lyt-2, or Lyt-3 antiserum and complement. Specificity was established by tests with C57BL/6 Lyt congenic mice and absorption studies with thymocytes. Similarly, the cytotoxicity of effector cells directed against semisyngeneic myeloma targets was reduced by Lyt-1, -2, or -3 antiserum and complement. Effector cell cytotoxicity against another semisyngeneic target was only marginally affected by Lyt-1 antiserum and complement, but was abolished by Lyt-2 or -3 antiserum and complement. It appears likely that cytotoxic T cells are a heterogeneous population with regard to Lyt-1 expression and that past studies indicating an apparent absence of Lyt-1 on cytotoxic T cells revealed a quantitative, not qualitative, feature of these cells. With regard to the activity of Lyt antisera in the absence of added complement, selective blocking of effector cell cytotoxicity for allogeneic and semisyngeneic targets was found with Lyt-2 and Lyt-3 antisera but not with Lyt-1 antiserum. The specificity of blocking was established by tests with Lyt congenic mice and absorption studies with thymocytes. With the exception of blocking by antisera to the H-2 haplotype expressed by the target cell, no effector cell blocking was observed with alloantisera or heteroantisera to a range of other cell surface molecules present on mouse lymphoid cells. One possibility to account for the selective blocking by Lyt-2 and Lyt-3 antisera is that Lyt-2,3 determinants on the surface of cytotoxic T cells have a close spatial relation to the T cell receptor.
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PMID:Cytotoxic T cells: Lyt phenotype and blocking of killing activity by Lyt antisera. 8 50

A 3-year-old female Siamese cat was admitted to a local animal hospital with a history of recent extreme lethargy and anorexia. A hemorrhagic tumor was removed from an area of oral buccal skin and diagnosed histopathologically as lymphosarcoma. Rapid physical deterioration occurred, and the cat became moribund 2 weeks after surgical operation. Necropsy revealed at least 200 spherical hemorrhagic neoplastic nodules attached to the omentum, mesentery, and peritoneum. Examination of histopathologic sections confirmed the striking characteristics of an extremely vascular and highly invasive malignant lymphoma, which was designated feline tumor No. 01 (FeT-01). There was no evidence of peripheral blood leukemia. Electron microscopic examination of tumor tissue revealed numerous viral particles having characteristics common to both feline leukemia virus (FeLV) and feline syncytium-forming virus (FeSFV). Primary cells and cultures propagated from tumor tissue were found to be negative or weakly positive for group-specific (gs) antigen by radioimmunoassay but strongly positive when assayed by indirect immunofluorescence. Co-cultivation of cells from tumor tissue, with normal prescreened feline embryo cells, revealed the presence of numerous FeSFV-like viral particles in the absence of C-type virus. A FeSFV was isolated from these passaged cells, with characteristics similar to FeSFV isolates previously described in the literature. The apparent presence of FeSFV in lymphosarcomatous tissue and the apparent absence of FeLV C-type particles in passaged cells indicate the need to make a more intensive study of the FeSFV group of viruses and the possible etiologic relationship to feline malignancies.
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PMID:An unusual case of feline leukemia and an associated syncytium-forming virus. 16 23

A 3-year-old child diagnosed as having acute lymphatic leukemia (ALL), developed meningeal leukemia 36 months after the onset of the disease. He was twice subjected to cranial irradiation plus intrathecal methotrexate (i.t. MTX). Skull radiology showed bilateral gyriform calcification of both cerebral hemispheres. Hematological relapse was first detected 5 years after diagnosis and the child died 5 months later. The most striking findings of a right frontal lobe biopsy and the postmortem examination were wide calcium deposits located in the cortex and in the adjacent white matter. Intense demyelination as well as areas of neuron poverty were apparent in the necropsy but in the biopsy specimen. The possible interrelationship between such deposition and cranial irradiation and/or i.t. MTX suggests a new iatrogenic disorder.
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PMID:Intracerebral calcifications in childhood lymphoblastic leukemia. A new iatrogenic disease? 41 41

A 3 1/2-year-old boy, during the course of acute lymphocytic leukemia presented clinical, roentgenological and ECG signs of myocarditis, which disappeared completely within 1 1/2 month. ECHO type 7 virus was isolated from the faeces during the acute stage of the disease and rise in ECHO 7 neutralizing antibodies was demonstrated in paired sera of the patient. This unusual pathogenicity of ECHO 7 virus could be explained with the impairment of the host resistance induced by leukemia and immunosuppressive therapy.
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PMID:Myocarditis associated with Echo type 7 infection in a leukemic child. 106 56

The activity of DNA-dependent RNA polymerase A and B in isolated nuclei of spleens of mice infected with Rauscher leukemia virus was studied. A 3-fold increase in the activity of both RNA-polymerases in leukemic spleens was established. Study of the properties of RNA-polymerase B from nuclei of spleens of mice infected with Rauscher virus in comparison with the enzyme from normal tissue revealed the existence of some specific features in the enzyme from leukemic cells. The nature of the increased activity of RNA-polymerase B in leukemic cells is discussed.
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PMID:[Activity of DNA-dependent RNA polymerases A and B in spleen nuclei of mice infected with Rauscher leukemia virus]. 125 55

A highly aggressive subclone of the human CALLA+C mu+ pre-B acute lymphoblastic leukemia (ALL) cell line NALM-6 (designated NALM-6-UM1) caused disseminated and fatal leukemia in CB.17 mice with severe combined immunodeficiency (SCID). An intravenous challenge with 1 x 10(6) (NALM-6-UM1 cells caused 15 of 27 (56%) SCID mice to become paraplegic at 31 +/- 2 days (median = 33 days) and 27 of 27 (100%) mice to die of disseminated leukemia at 38 +/- 1 days (median = 39 days). We used this SCID mouse model of aggressive human pre-B ALL to evaluate the in vivo antileukemic efficacy of B43 (anti-CD19)-pokeweed antiviral protein (PAP) immunotoxin. A 3-day treatment with nontoxic doses of B43-PAP markedly reduced the incidence of paraplegia and improved event-free survival (EFS) in SCID mice challenged with 1 x 10(6) NALM-6-UM1 pre-B ALL cells, as reflected by significantly higher cumulative proportions of mice free of paraplegia or alive at 1 to 7 months, as compared with phosphate-buffered saline (PBS) treated control mice. The Kaplan-Meier estimates and standard errors of the probability of developing paraplegia after inoculation of 1 x 10(6) NALM-6-UM1 cells was 64% +/- 10% for PBS-treated mice (median time to paraplegia = 37 days) (N = 27), 18% +/- 8% for mice treated with 15 micrograms B43-PAP (5 micrograms/mouse/d x 3 days) (N = 23) and 5% +/- 5% for mice treated with 30 micrograms B43-PAP (10 micrograms/mouse/d x 3 days) (N = 21). While 27 of 27 PBS-treated control SCID mice died of leukemia at 38 +/- 1 days (range = 24 to 54 days), only 16 of 44 B43-PAP-treated mice developed leukemia at 74 +/- 12 days (range = 30 to 182 days), consistent with greater than or equal to 6 logs kill of clonogenic NALM-6-UM1 cells in 64% of SCID mice. The Kaplan-Meier estimates and standard errors of the probability of long-term EFS after inoculation of 1 x 10(6) NALM-6-UM1 cells were 65% +/- 10% for mice treated with 15 micrograms B43-PAP and 60% +/- 11% for mice treated with 30 micrograms B43-PAP with a median survival time of greater than 7 months for both groups. In contrast, neither unconjugated B43 monoclonal antibody nor the anti-T-cell immunotoxin G17.2 (anti-CD4)-PAP decreased the incidence of paraplegia or improved EFS.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:In vivo efficacy of B43 (anti-CD19)-pokeweed antiviral protein immunotoxin against human pre-B cell acute lymphoblastic leukemia in mice with severe combined immunodeficiency. 137 67

Three ets family members, v-ets, spleen focus forming virus proviral integration 1/Pu.1, and Friend leukemia integration 1 (Fli-1), were shown to be involved in retroviral mediated acute leukemias suggesting that ets family members play a crucial role in transformation. Mouse Fli-1 was shown to be involved in 75% erythroleukemias induced by Friend murine leukemia virus suggesting the possibility that Fli-1 may play a critical role in cellular transformation. Since Fli-1 maps to the mouse chromosome region syntenic with human chromosome 11q23-24, it is tempting to speculate that human Fli-1 may be involved in human sarcomas, leukemias, and lymphomas involving human chromosome 11q23-24. We have isolated complementary DNA clones representing the human homologue of Fli-1 gene. Nucleotide sequence analysis revealed that the human Fli-1 gene codes for a 452-residue protein the predicted amino sequence of which shows 80% homology to the human erg-2 protein previously described. A 3.5-kilobase transcript of the human Fli-1 gene was observed in different cells. Sequence analysis revealed two domains of ets homology, one at the 5' and the other at the 3' end of the Fli-1 gene. This 3'-ets homology domain, which is mainly responsible for DNA binding activity, is seen in all the ets family members; however, the 5'-ets homology region is conserved in only five genes, Fli-1, c-ets-1, ets-2, GABP-alpha, and erg, suggesting a common biological function which is shared among these genes. Interestingly, mouse and human Fli-1 transcripts contain highly homologous 5'-untranslated region suggesting that this conserved region may play an important role in the posttranscriptional regulation of the Fli-1 transcript.
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PMID:Structure and expression of human Fli-1 gene. 139 11

First described on pre-B leukemia cells, the common acute lymphoblastic leukemia antigen (cALLa) is also expressed on glioma cells in vitro. Its identity to neutral endopeptidase (NEP) (E.C.3.24.11) was corroborated by our finding that cALLa positive glioma cells had NEP activity. To study cALLa/NEP distribution on glial tumours in vivo, we examined 76 brain tumour biopsies by immunostaining techniques on frozen tissue sections using anti-cALLa (FAH99) and anti-NEP (135 A 3) monoclonal antibodies. We found that 96% of grade 4 gliomas (25/26) expressed NEP. Whereas only 45% (4/9) of grade 3 or anaplastic astrocytomas did. In low grade gliomas, we found 2 positive tumours out of 21 tested (10%). Double immunostaining procedures revealed that NEP was co-expressed with GFAP. However no NEP could be detected on non-glial brain tumours nor on reactive astrocytes. These results suggest that cALLa/NEP expression could be linked to malignant progression of gliomas.
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PMID:Expression of cALLa/NEP on gliomas: a possible marker of malignancy. 153 80

A 3-year-old boy was referred to our hospital in September 1985, because of pancytopenia. His bone marrow was normocellular with 18% blasts, which had Auer rod and were positive for peroxidase staining. A diagnosis of refractory anemia with excess blasts in transformation was made according to FAB criteria. Chromosome analysis of bone marrow cells showed normal male karyotype. He attained complete remission with aclarubicin and BH-AC and continued it until August 1987 when pancytopenia and hypoplastic bone marrow developed. Chromosome analysis of bone marrow cells showed normal male karyotype and gene analysis revealed germ-line configuration of breakpoint cluster region (bcr). Overt leukemia developed in May 1988 when his WBC count increased to 60, 600/microliters with 91% blasts, which were negative for peroxidase staining, positive for anti-Ia and CDw 41 by cell surface analysis, and positive for ultrastructurally demonstrable platelet peroxidase. A diagnosis of megakaryocytic leukemia was made. Chromosome analysis of bone marrow cells showed 46, XY, t(9;22) (q34;q11) and gene analysis revealed rearrangement of bcr. He died in November 1988. Our results and review of literature suggest that late appearing ph1 chromosome and rearrangement of bcr may occur in a variety of hematologic malignancies and influence the course of disease.
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PMID:[Myelodysplastic syndrome in a child which developed into megakaryocytic leukemia with late appearing Ph1 chromosome and rearrangement of breakpoint cluster region]. 221 96

A 3.0-kilobase-pair Epstein-Barr virus (EBV) DNA segment necessary for lymphocyte immortalization encodes at least part of a nuclear protein (EBNA2) which is characteristically expressed in latently infected, immortalized cells. A 1.5-kilobase open reading frame within this DNA segment has now been inserted into a murine leukemia virus (MuLV)-derived expression vector (pZIP-NEO-SV(X)1) which provides for transcription of heterologous DNA but not for translational start. Transfection of the recombinant DNA into NIH 3T3 cells resulted in expression of a full-sized EBNA2 which localized to the cell nucleus. Significant new evidence is thereby provided that this 1.5 kilobase open reading frame includes a translational start site and encodes the entire EBNA2 protein. Transfection of the recombinant DNA into a helper cell line (psi am22b) providing amphotropic MuLV-packaging functions resulted in the release of a recombinant MuLV carrying the EBNA2 gene. This recombinant virus can infect rodent cells and convert them to stable EBNA2 expression. Rat-1 cells infected with the MuLV EBNA2 recombinant expressed EBNA2 and grew more rapidly in medium supplemented with 1 or 0.5% fetal calf serum than did Rat-1 cells infected with MuLV vector lacking EBNA2. The Rat-1 cells expressing EBNA2 remained contact inhibited, anchorage dependent, and nontumorigenic in nude mice. Different EBV isolates have one of at least two EBNA2 alleles. Despite divergence between the two alleles, a human serum recognized the prototype EBNA2 allele (EBNA2A) as well as the variant EBNA2B allele characteristic of some Burkitt tumor EBV isolates. The EBNA2B allele was also expressed from the MuLV-derived vector. The reproducible expression of EBNA2A or EBNA2B from these recombinant vectors will facilitate analysis of the EBNA2A and EBNA2B phenotypes.
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PMID:Expression of the Epstein-Barr virus nuclear protein 2 in rodent cells. 242 68


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