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)

Equine infectious anemia virus (EIAV) has a density of 1.154 g/cm3 in sucrose a high-molecular-weight RNA similar in size to Rauscher murine leukemia virus, and an internal virion reverse transcriptase that utilizes the synthetic RNA template poly(rA) but not the synthetic DNA template poly(dA), both with (dT)12 as primer. Although capable of utilizing manganese at low concentrations (approximately 0.1 mM), EIAV reverse transcriptase showed highest activity in the presence of 9 mM magnesium. The major protein of EIAV has a slightly lower molecular weight than the comparable protein of type C viruses and co-electrophoresed with 125I-labeled p25 of Mason-Pfizer monkey virus. A reference horse serum with antibodies to the major EIAV protein reacted only with EIAV and not with other type C or non-type C retraviruses. Reciprocally, a broadly reactive serum to type C virus p30s and specific sera to a variety of non-type C retraviruses did not react with EIAV. We recommend the inclusion of EIAV in the family Retraviridae.
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PMID:Equine infectious anemia virus: evidence favoring classification as a retravirus. 6 Dec 83

The major internal polypeptide of the bovine leukemia virus (BLV) was purified to homogeneity with the use of gel filtration and affinity chromatography. Like previous results, the protein had a molecular weight of 25,000 daltons as determined by electrophoresis in polyacrylamide gels with sodium dodecyl sulfate. More than 90% of the 125I-labeled protein was precipitated by bovine sera that reacted in immunofluorescence tests with acetone-fixed BLV-infected cells. In contrast, minimal precipitation (less than 5%) was observed with sera from 36 cattle in leukemia-free herds; these sera, negative by immunofluorescence, included six samples that had high titers of antibodies to the foamy-like bovine syncytia virus (BSV). Antisera prepared against several other oncornaviruses or the Mason-Pfizer monkey virus (M-PMV) did not bind the BLV p25 protein. Conversely, the labeled p30 polypeptides of several oncornaviruses tested did not react with bovine sera that had high titers of antibodies to BLV p25. Competitive radioimmunoassay(s) (RIA) also failed to detect cross-reactions between BLV p25 protein and the internal polypeptides of other mammalian and avian oncornaviruses, M-PMV, or foamy-like BSV. The RIA for BLV p25 antigen was also highly sensitive and specific for the detection and quantitation of the antigen in virus preparations and cell homogenates.
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PMID:Detection, quantitation, and characterization of the major internal virion antigen of the bovine leukemia virus by radioimmunoassay. 6 63

Radioimmunoassay of J-96 virus and an extract of J-96 cells in the homologous and heterologous systems aimed at detecting antigenic determinants of p25 of Mason-Pfizer virus, as well as group-specific and interspecies antigenic determinants p30 of Rauscher leukaemia virus demonstrated that (1) J-96 virus contains a major internal protein immunologically identical with p25 protein of Mason-Pfizer virus based on the antigenic determinants detectable by the radioimmunoassay used; and (2) no interspecies antigenic determinants characteristic of the major internal protein of mammalian type C viruses were detectable in the J-96 virus or the J-96 cell extract.
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PMID:Radioimmunoassay of type D oncovirus from continuous J-96 cells. 8 Sep 55

A nuclear matrix (NM)-associated region (MAR) of the protooncogene c-myc is identified in a human leukemia cell line (HL-60). A binding assay between isolated NM and 32P-end-labeled c-myc fragments in the presence of unlabeled competitors was used, and a 3'-end DraI/DraI fragment of 172 base pairs containing the first of the two polyadenylation [poly(A)] signals was identified as an in vitro MAR. Direct detection of endogenous c-myc fragments remaining NM bound after restriction digestion was used, and an in vivo MAR has been identified as the ClaI/EcoRI 1.4-kilobase pair fragment containing the 172-base pair in vitro MAR fragment. In addition, a nuclear protein (Mr = 25,000, p25) demonstrating preferential binding to the 172-base pair c-myc MAR has been identified and partially purified. This protein is diminished in the nuclei of the cells induced by phorbol ester to undergo macrophage differentiation. Footprint analysis shows that p25 binds to two regions of the 172-base pair fragment. One contains the first of two poly(A) addition signals and a topo II box-like sequence, and the other (AATTTCAATCCTAGTA) is 17 base pairs downstream of the first poly(A) signal.
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PMID:Identification of a nuclear matrix-associated region of the c-myc protooncogene and its recognition by a nuclear protein in the human leukemia HL-60 cell line. 218 83

Human T-cell leukemia virus (HTLV) type I-related endogenous sequences (HRES) have been cloned from a human genomic library. HRES-1/1 is present in DNA of all normal donors examined. By nucleotide sequence analysis, HRES-1/1 contains two potential open reading frames capable of encoding a p25 and a p15. A 684 bp flanking region 5' from the first ATG codon of p25 contains a TATA-box, a poly-adenylation signal, a putative tRNA primer binding site, and inverted repeats at locations which are typical of a retroviral long terminal repeat. Phylogenetic analysis suggests that HRES-1/1 entered the genome in primates, presumably as an exogenous retrovirus. From the deduced amino acid sequence of HRES-1/1 p25, residues 6-36 show a sequence homology of 32% and 39% to gag region segments of HTLV-I and HTLV-II, while residues 104-139 display a sequence homology of 33% and 28% to the gag regions of human immunodeficiency virus type 2 (HIV-2) and feline sarcoma virus (FSV), respectively. This suggests that the original exogenous virus infecting primate may be chimeric in structure. The HRES-1/1 genomic locus is transcriptionally active in lymphoid cells, melanoma cells, and embryonic tissues.
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PMID:Detection and cloning of new HTLV-related endogenous sequences in man. 278 Mar 12

This report demonstrates a case of acute megakaryoblastic leukemia evolving in a patient with idiopathic myelofibrosis with myeloid metaplasia. A presumptive diagnosis was made by cytochemical stains, alpha-naphthyl acetate esterase, and alpha-naphthyl butyrate esterase. The diagnosis was established by electron microscopic platelet peroxidase studies of the peripheral blood blast cells and supported by flow cytometry and immunoalkaline phosphatase studies. Specific monoclonal antibodies directed against platelet glycoproteins Ib (6D1) and IIb/IIIa (10E5), which have not been described frequently in analyzing leukemia, were used for flow cytometry and direct immunoalkaline phosphatase technique. Cytogenetic studies demonstrated a deletion of the long arm of chromosome 6 with breakpoints at bands q15 and q23, and ring chromosome 6 (p25, q27). The diagnosis of megakaryoblastic leukemia requires accurate cytochemical stains, platelet peroxidase by electron microscopic examination, and studies employing specific monoclonal antibodies directed against platelets and megakaryoblasts. The exact origin of the circulating megakaryoblasts in these cases is not known and needs additional investigation.
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PMID:Diagnosis of acute megakaryoblastic leukemia by flow cytometry and immunoalkaline phosphatase techniques. Utilization of new monoclonal antibodies. 282 18

Chromosome analysis was performed on 1 patient with diffuse lymphoma of mixed type by histologic diagnosis and on 7 patients with the acute type of adult T-cell leukemia (ATL). Specific abnormalities in chromosome 14 at break band q11 with the assigned locus of the alpha-chain gene of the T-cell antigen receptor were identified in 6 of 8 patients. Inv(14) (q11q32) was found in 2 patients and translocation of chromosome 14 at break band q11 was observed in 4. Donor chromosomes involved in translocation of the 14q11 varied, i.e., chromosomes 3, 7 or X, with the exception of one patient whose donor chromosome origin could not be determined. The breakpoint in chromosome 3 was in band p25, a region reported to include the locus of the c-raf-I oncogene. In chromosome 7, it was in band p11, a region reported to include the locus of the c-erb-B oncogene, and in the sex chromosome X, it was in band q11. One patient also had a chromosome 14 aberration at break band q32. Of the 2 remaining patients, one had lost chromosome 14 and the other had an isochromosome 14q. Our observation and other reported findings suggest that the rearrangement of chromosome 14 at break band q11 is specific for lymphoma-type or acute-type ATL patients, and aberrations of proto-oncogene expression or the coding sequence by recombination involving a T-cell antigen receptor gene due to chromosome inversion or chromosome translocation may play an important role in T-cell neoplasia including ATL.
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PMID:Specific abnormalities of chromosome 14 in patients with acute type of adult T-cell leukemia/lymphoma. 288 76

A B-cell line having translocations of chromosome 14 at break band q11 (the assigned locus of the alpha-chain gene of the T-cell antigen receptor) and chromosome 3 at break band p25 (the assigned locus of the c-raf-1 oncogene) was established from peripheral blood leukocytes of an adult T-cell leukemia (ATL) patient. The same chromosome 14 aberration at break band q11 and chromosome 3 aberration at break band p25 were also found in fresh T-cell leukemia cells. The B-cell line is surface immunoglobulin (sIg)+, immunoglobulin gene rearrangement+, ATL-specific antigen (ATLA)+, HTLV-1 proviral genome+, Epstein-Barr virus (EBV)-associated nuclear antigen (EBNA)+ and the EBV DNA genome+. The fresh T-leukemic cells were T-cell receptor gene rearrangement+, the HTLV-1 proviral genome+ and EBV DNA genome.
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PMID:A B-cell line having chromosome 14 aberration at break band q11 derived from an adult T-cell leukemia patient. 289 57

Cytogenetic studies are reported on 17 T-cell malignant lymphomas (ML) including six cutaneous T-cell malignant lymphomas (CTCL). Due to the low incidence of rearrangements on bands where the T-cell receptor genes are located, other cases reported in the literature were analyzed in order to estimate the most frequent chromosomal breakpoints in ML, CTCL, and adult T-cell leukemia-lymphoma. Besides chromosomes 1 and 6q, 14q11, 7p15p21, and 7q32q35, the most frequent rearrangements involved bands 14q32, 2p11-p14, 2p23-p25, 17cen, 9p21p23, and 10p13p15. These results show that molecular studies must be concentrated on these chromosomal regions in order to identify the DNA sequences that may be involved in T-cell malignancies.
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PMID:Cytogenetics of T-cell malignant lymphoma. Report of 17 cases and review of the chromosomal breakpoints. 306 Feb 49

Lymphadenopathy associated virus (LAV) is a novel human retrovirus first reported in 1983. It was isolated from the lymph node lymphocytes of a French homosexual patient with generalized hyperplasic lymphadenopathy. Subsequently LAV was isolated from patients with frank acquired immune deficiency syndrome (AIDS) coming from all the different high-risk groups, while anti-LAV antibodies were detected equally in individuals from all "at-risk" groups. Such a profile is consistent with the virus being the major etiological agent of AIDS. Furthermore its biological properties, namely its cytopathic effect in vitro, its T4-cell tropism as well as the role of the T4 molecule in virus infection explain, at least in part, the pathophysiology of AIDS. The major core (gag) proteins are p18, p25, and p13 which are products of a Pr55 precursor. The major envelope (env) glycoprotein is unusually large (gp110) for a retrovirus and comparable to those of the lentiviruses. Recently the virus has been molecularly cloned. The genome is 9.2 kb long, longer than any other known replication competent retrovirus apart from the lentiviruses. The absence of molecular hybridization between cloned LAV and human T-cell leukemia/lymphoma virus (HTLV) genomes compounds the original and extensive differences noted between these viruses and demonstrates that LAV is a prototype of a new class of human retrovirus.
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PMID:Lymphadenopathy associated virus and its etiological role in AIDS. 610 Jun 50


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