Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Friend murine leukemia helper viruses (F-MuLV) 57 and B3 were indistinguishable by genomic structural analyses with RNase T1-resistant oligonucleotide fingerprinting and by antigenic reactivity with a panel of 31 monoclonal antibodies directed against murine leukemia viruses. Nevertheless, F-MuLV 57 and B3 had strikingly different virulences. Approximately 2 months after inoculation, IRW and NFS/N mice inoculated as newborns with F-MuLV 57 had gross splenomegaly caused by erythroid proliferation. In contrast, an equivalent dose of F-MuLV B3 induced spleen or lymph node enlargement 4 to 13 months after inoculation. Although most cases of spleen enlargement in F-MuLV B3-inoculated mice were due to erythroid proliferation, lymphoid or myeloid proliferation was also frequently observed. The replication of both F-MuLV 57 and B3 was equally efficient, and both viruses generated recombinant dual-tropic mink cell focus-forming (MCF) viruses with the same kinetics and efficiency. Moreover, MCF viruses induced by F-MuLV 57 and B3 had the same antigenic patterns. Therefore, the ability of F-MuLV to induce early splenomegaly did not correlate with the generation of recombinant MCF viruses.
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PMID:Analysis of two strains of Friend murine leukemia viruses differing in ability to induce early splenomegaly: lack of relationship with generation of recombinant mink cell focus-forming viruses. 300 61

Mouse C127I cells were transformed with a chimeric plasmid consisting of bovine papillomavirus DNA and human granulocyte-colony-stimulating factor (G-CSF) cDNA placed under the control of the SV40 early promoter. The transformed cells secreted constitutively a high level of human G-CSF, 10-20 micrograms/ml in a low-serum medium. The secreted G-CSF has been purified to homogeneity by a two-step procedure including gel filtration and hydrophobic column chromatography. The purified recombinant G-CSF runs as a single band with an apparent Mr of 19,000 on a polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. This value corresponds to that of the native human G-CSF purified from the medium conditioned by human carcinoma CHU-2 cells. The recombinant human G-CSF was as active as native G-CSF in vitro in supporting proliferation of mouse NFS-60 cells and stimulating colony formation from human as well as mouse bone marrow cells. When the recombinant human G-CSF was subcutaneously administrated into mice, a remarkable stimulation of granulopoiesis and splenomegaly was observed.
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PMID:Characterization of recombinant human granulocyte-colony-stimulating factor produced in mouse cells. 303 99

Cellular ras oncogenes transduced by retroviruses carry mutations in amino acids 12, 59 and 122. Similar mutations have been observed in ras oncogenes activated during induction of neoplasia in both humans and experimental animals. The unmutated normal rat or human c-Ha-ras-1 genes have the ability to transform NIH 3T3 cells in culture when activated by a RNA synthesis promoter. These findings raise the question of whether the mutations are necessary for the ras oncogenes to induce the neoplastic phenotype in vivo. To address this question, we inserted the normal human c-Ha-ras-1 or its mutated counterpart EJ/T24 bladder carcinoma oncogene independently into a retrovirus vector derived from the M1 strain of Moloney murine sarcoma virus (MoMuSV). Both recombinant clones induced foci of transformed cells in an NIH 3T3 cell transfection assay. Infectious virus particles were rescued from cloned transformants carrying a single copy of the integrated provirus using the nonpathogenic amphotrophic wild mouse leukemia virus (WMLV) as helper. The pseudotypes rescued from the EJ/T24-containing transformants had higher titers than the normal c-Ha-ras-1 pseudotypes as determined by a focus assay and gave rise to larger and earlier detected foci upon infection of NIH 3T3 cells. The two pseudotypes were tested for in vivo pathogenicity by inoculation into newborn NFS mice and were compared to the pseudotype WMLV/Harvey murine sarcoma virus (HaMuSV) (positive control) and WMLV (negative control). While the WMLV/EJ/T24 and the WMLV/HaMuSV pseudotypes induced erythroleukemias and sarcomas with a latency period of 6-9 weeks, the WMLV/c-Ha-ras-1 pseudotype induced only mild splenomegaly. As expected the WMLV negative control induced no pathology. Tumor-bearing animals that were not euthanized at 6-9 weeks died within 2-3 months following virus inoculation.
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PMID:Pathogenicity of retroviruses containing either the normal human c-Ha-ras1 gene or its mutated form derived from the bladder carcinoma EJ/T24 cell line. 384 94

An NFS/N mouse inoculated at birth with an ecotropic murine leukemia virus (MuLV) obtained from wild mice (Cas-Br-M MuLV) developed a lymphoma after 18 weeks. An extract prepared from the lymphomatous spleen was inoculated into newborn NFS/N mice, and these mice developed erythroleukemia within 9 weeks. Spleens from the erythroleukemic mice contained ecotropic and mink cell focus-inducing (MCF) MuLVs; however, when these viruses were biologically cloned and reinoculated into newborn NFS/N mice, no erythroleukemia was induced. In contrast, cell-free extracts prepared from the erythroleukemic spleens induced erythroleukemia within 5 weeks. Analysis of cell-free extracts prepared from the erythroleukemic spleens showed that they contained a viral species that induced splenomegaly and spleen focus formation in adult mice, with susceptibility controlled by alleles at the Fv-2 locus. The spleen focus-forming virus coded for a 50,000-dalton protein precipitated by antibodies specific to MCF virus gp70. RNA blot hybridization studies showed the genomic viral RNA to be 7.5 kilobases and to hybridize strongly to a xenotropic or MCF envelope-specific probe but not to hybridize with an ecotropic virus envelope-specific probe. The virus described here appears to be the fourth independent isolate of a MuLV with spleen focus-forming activity.
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PMID:Identification of a spleen focus-forming virus in erythroleukemic mice infected with a wild-mouse ecotropic murine leukemia virus. 629 59