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 molecularly cloned unintegrated viral DNA of the BALB/c endogenous N-tropic and B-tropic murine leukemia retroviruses and in vitro passaged N-tropic Gross (passage A) murine leukemia retroviruses. Recombinant genomes were constructed in vitro by exchanging homologous restriction enzyme fragments from N- or B-tropic parents and subsequent recloning. Infectious virus was recovered after transfection of these recombinant genomes into NIH-3T3 cells and cocultivation with the Fv-1 nonrestrictive SC-1 cells. XC plaque assays of recombinant virus progeny on Fv-ln and Fv-lb cells indicated that the Fv-l host range was determined by sequences located between the BamHI site in the p30 region of the gag gene (1.6 kilobase pairs from the left end of the map) and the HindIII site located in the pol gene (2.9 kilobase pairs from the left end of the map).
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PMID:Reversal of Fv-1 host range by in vitro restriction endonuclease fragment exchange between molecular clones of N-tropic and B-tropic murine leukemia virus genomes. 631 Jan 40

A recombinant DNA clone, named AL10, that contains murine leukemia virus (MuLV) related sequences was isolated from BALB/c mouse chromosomal DNA and examined in detail. Restriction endonuclease mapping revealed that the 10.5 kbp EcoRI insert consists of a 3.6 kbp left flanking cellular DNA region and a 6.9 kbp MuLV-related region that has a typical proviral LTR-gag-pol-env structure up to the EcoRI site in the env gene region. Comparison of the AL10 map with ecotropic and xenotropic virus isolates revealed many common restriction sites in the LTR and pol gene regions, but much fewer in the leader and gag regions. A stretch of 1,700 nucleotides containing the cellprovirus junctional region was sequenced and revealed transcriptional consensus signals and other structural features characteristic of MuLV LTRs, as well as two distinctive features: (a) a sequence of approximately 170 bp with direct and inverted terminal repeats not seen in infectious MuLV LTRs was identified in the U3 region between the "enhancer" region and the "CAT" box. This novel segment or its homologous sequences appear to be present in most of the endogenous MuLV-related LTRs and in other chromosomal locations of the mouse (b) The tRNA primer binding site is not complementary to proline tRNA, the primer for all known MuLVs, but is a 17/18 match with rat glutamine tRNA. The integration site of AL10 provirus was in a unique DNA region but contained an "Alu"-like short interdispersed repeat in the 5' adjacent cellular region. The AL10 proviral integration found in BALB/c was also apparent in RFM, AKR and SENCAR mouse cells but not in cells of NFS/N, C3H, HRS/J, SC-1, and a California Lake Casitas wild mouse.
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PMID:A novel sequence segment and other nucleotide structural features in the long terminal repeat of a BALB/c mouse genomic leukemia virus-related DNA clone. 631 May 6

The murine leukemia viruses (MuLVs) have different host ranges and were originally designated N-tropic and B-tropic if they replicated preferentially in vitro on NIH and BALB/c fibroblasts, respectively. It was later found that N-tropic MuLVs were in fact restricted in BALB/c cells, that B-tropic MuLVs were restricted in NIH cells, and that both viruses were restricted in (BALB X NIH) F1 cells. A single gene, Fv-1, with two alleles, Fv-1b and Fv-1n, determines this dominant restriction. A virus-encoded protein seems to carry the viral host range determinant which is recognized by the Fv-1 gene product. To map the viral DNA sequences encoding this determinant, we constructed viral DNA recombinants in vitro between the cloned infectious viral DNA genomes from BALB/c N-tropic and B-tropic MuLVs. Infectious recombinant MuLVs were recovered by microinjecting these recombinant DNAs into murine Fv-1- SC-1 cells and were subsequently tested in vitro for their host ranges (N- or B-tropic). We found that a short 302-base pair 5'-end fragment was necessary and sufficient to confer a specific host range to a recombinant. Our sequencing data revealed that this fragment codes for amino acid sequences in gag p30. They also showed that only two consecutive amino acid differences, Gln-ArgN- and Thr-GluB-, in p30 are responsible for the N- and B-tropic host ranges of the BALB/c MuLVs, respectively. Therefore, it appears that the Fv-1b and Fv-1n gene products can discriminate between these two p30 amino acid sequences.
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PMID:Physical mapping of the Fv-1 tropism host range determinant of BALB/c murine leukemia viruses. 631 67

A family of recombinant mink cell focus-forming viruses (MCF) was derived by inoculation of NFS mice with a Friend murine leukemia virus, and their genomes were analyzed by RNase T1-resistant oligonucleotide fingerprinting. The viruses were obtained from the thymuses and spleens of preleukemic and leukemic animals and were evaluated for dualtropism and oncogenicity. All these isolates induced cytopathic foci on mink cells but could be classified into two groups based on their relative infectivities for SC-1 (mouse) or mink (ATCC CCL64) cells. One group of Friend MCFs (F-MCFs) (group I) exhibited approximately equal infectivities for SC-1 and mink cells, whereas a second group (group II) infected mink cells 1,000- to 10,000-fold more efficiently than SC-1 cells. Structural analyses of the F-MCFs revealed that group I and group II viruses correlated with recombination of Friend murine leukemia virus with two distinct, but closely related, endogenous NFS proviral sequences. No correlation was found between the type of F-MCF and the tissue of origin or the disease state of the animal. Furthermore, none of the F-MCF isolates were found to be oncogenic in NFS/N or AKR/J mice. F-MCFs of both groups underwent extensive substitution of ecotropic sequences, involving much of the gag and env genes of group I F-MCFs and most of the gag, pol, and env genes of group II F-MCFs. All F-MCF isolates retained the 3' terminal U3 region of Friend murine leukemia virus. Comparison of the RNAs of the F-MCFs with RNAs of MCFs derived from NFS.Akv-1 or NFS.Akv-2 mice indicated that the F-MCFs were derived from NFS proviral sequences which are distinct from the sequences contained in NFS.Akv MCF isolates. This result suggested that recombination with particular endogenous proviral sequences to generate MCFs may be highly specific for a given murine leukemia virus.
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PMID:Generation of mink cell focus-forming viruses by Friend murine leukemia virus: recombination with specific endogenous proviral sequences. 642 51

The SC-1 antigen, identified by thymus-absorbed rabbit anti-mouse brain antiserum, is present on multipotential stem cells. Its presence on cells of the T lineage has been examined by immunofluorescence, and we have demonstrated that it is also a marker for thymic development. Although it is present on the majority of fetal and neonatal thymocytes, its expression declines rapidly and, as early as 1 mo after birth, adult levels are reached. In normal animals, these do not change during adult life, even in mice destined to develop a T cell leukemia. SC-1 does reappear transiently on cells in the regenerating thymus of sublethally irradiated mice. Although the antigen is not associated with preleukemic changes in the thymus, it is expressed on some cells of all spontaneous T lymphomas, and it is uniformly present on tissue culture lines of T cell lymphomas.
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PMID:Serologic identification of early members of the T cell lineage. 680 Nov 21

A xenoantiserum to murine B16 melanoma cells was developed by immunizing rabbits with cultured B16 melanoma cells. This antiserum could, after extensive absorption with normal C57BL/6 mouse tissues, react with syngeneic (B16) and allogeneic (HP) melanomas as well as with other murine neoplasms, including syngeneic 75S adenocarcinoma, allogeneic myeloma and leukemic T cell lines. The antiserum also cross-reacted with syngeneic fetal fibroblasts and with an allogeneic fetal fibroblast cell line (SC-1) either uninfected or infected with murine leukemia virus (MuLV). Immunoprecipitated material from B16 melanoma cell-surface glycoproteins that had been labeled with [125I] by lactoperoxidase and purified by a Lentil lectin column was analyzed by one-dimensional SDS- and two-dimensional polyacrylamide gel electrophoresis, which disclosed an acidic glycoprotein with a molecular weight (mol. wt) of 90 K daltons. Absorption studies suggested that the 90 K mol. wt gylcoprotein represented the oncofetal moiety expressed in murine medanoma, carcinoma and fetal tissues. When the amount of this antigen in developing C57BL/6 mouse fetuses was measured by absorption assays, we found that it was expressed strongly in those fetuses just before birth. Binding and absorption studies demonstrated that the 90 K mol. wt glycoprotein, while being expressed on a variety of fetal and neoplastic cells in mice, did not exist at detectable levels in normal tissues of adult C57BL/6 mice, including tissues of the thymus, lymph node, spleen, liver, brain, lung and kidney.
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PMID:Identification of an oncofetal antigen (gp90) on murine B16 melanoma cells. 688 31

The leukemogenic activity of Gross murine leukemia virus adapted to rats was tested in W/Fu rats and NIH/Swiss mice. All animals infected with this virus developed thymic and nonthymic T-cell leukemia with a short latency period. It was observed that cell-free extracts from thymic lymphoma tissue of mice and rats, induced by either Gross murine leukemia virus or Gross murine leukemia virus adapted to rats, consisted of both small-plaque-forming and large-plaque-forming viruses, as determined by the XC plaque test. MCF-type virus was found in these virus complexes. Transformed cell foci were induced in SC-1 cell layers by double infection of the cloned MCF-type virus and an ecotropic virus. SC-1 cells containing transformed cell foci were shown to be tumorigenic upon inoculation into nude mice. The formation of transformed cell foci in mink lung cells was also observed after double infection with the cloned MCF-type virus and a xenotropic virus. The possible mechanism of leukemogenesis by endogenous viruses is discussed.
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PMID:Leukemogenicity and cell transformation mechanisms in vitro by Gross murine leukemia virus: analysis of virus subpopulations. 724 57

Virus-induced cell fusion of the fusion-from-without type was observed in SC-1 cells infected with Moloney murine leukemia virus when grown in NIH 3T3 cells. Replication-competent virus mutants with altered surface protein gp70 were examined. Fusion mutations were found in the proline-rich region of gp70. They acted on a step after binding and before or during endocytosis. The fusion mutants had an altered gp70 isomer pattern, presumably caused by different glycosylation. Other mutants with deleted glycans were analyzed, and some which also showed defective fusion were found. The interrelationship of the proline-rich region, glycosylation, and fusion is discussed.
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PMID:A domain of murine retrovirus surface protein gp70 mediates cell fusion, as shown in a novel SC-1 cell fusion system. 751 60

Specific hybridization primers for the PCR assay were developed to detect the presence of the ecotropic, xenotropic, and mink cell focus-forming classes of murine leukemia viruses (MuLVs) in samples derived from cultured cells and cell-free supernatants. The primers, which were tested against reference viruses from all three classes and two subclasses and accurately identified each class present, were used to characterize the endogenous expression of MuLV-related sequences in a number of murine and mink cell lines. Two murine/murine hybridomas were shown to contain expressed retroviral sequences from all three classes. The murine cell lines SC-1, Balb/c 3T3, and NIH 3T3, were found to constitutively express sequences from many of the MuLV classes. These MuLV-related sequences were not expressed in the Mus dunni or mink lung cell lines. When these primers were used in a quantitative PCR assay to determine the retroviral content of hybridoma supernatants, the values were less variable than those obtained by transmission electron microscopy (TEM). This assay can be adapted to detect and quantitate any viral contaminant in cell culture supernatants, ascites fluids, process validation samples, and final products.
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PMID:A reverse transcriptase-polymerase chain reaction assay for the detection and quantitation of murine retroviruses. 769 Feb 34

TR1.3 is a Friend-related murine leukemia virus that has been shown to cause intracerebral hemorrhages and neurologic disease due to infection and subsequent cytopathology of cerebral vessel endothelium. A striking feature of this pathology is the formation of endothelial cell syncytia. The pathogenesis of this disease has now been mapped to a single amino acid substitution of tryptophan to glycine in the variable region of the envelope protein. This same mutation enabled TR1.3 to form syncytia and retard cell proliferation in vitro in the SC-1 mouse embryoblast line but did not affect the pH dependence of viral entry. These results demonstrate that subtle molecular changes in retroviral env genes can induce both syncytium formation and overt clinical disease.
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PMID:A point mutation in the env gene of a murine leukemia virus induces syncytium formation and neurologic disease. 793 35


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