Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Permanent cell lines have been established from twelve diffuse histiocytic lymphomas (SU-DHL-1 to -12), three American Burkitt's lymphomas (SU-AmB-1 to -3), two acute lymphoblastic leukemias (SU-ALL-1 and -2), and three diffuse undifferentiated lymphomas (SU-DUL-1, -2, and -3). The cultured cells displayed neoplastic characteristics, as manifested by heterotransplantability in congenitally athymic nude mice and by the presence of cytogenetic abnormalities in early passage generations. Functional and marker studies revealed that the three American Burkitt's lymphomas, as well as several of the diffuse histiocytic and undifferentiated lymphomas, were of B-lymphocytic origin, whereas the two acute lymphoblastic leukemias were both of T-lymphocytic origin. Two of the cell lines, SU-DHL-1 and -2, appeared to be of true histiocytic origin; two others exhibited no markers and were designated as "null" cells. All ten of the DHL cell lines studied to date, as well as SU-DUL-1, have been devoid of Epstein-Barr virus (EBV) genomes by the EBNA test, whereas two of the three American Burkitt's lymphoma cell lines were positive. Spontaneous production of a C-type RNA virus was first detected in post-mitochondrial cytoplasmic fractions and culture fluids of the SU-DHL-1 cell line. Screening assays for the detection of reverse transcriptase-positive particles in the culture fluids of the other cell lines indicate that eight of the fifteen cell lines tested to date have spontaneously initiated C-type RNA virus production. After partial purification by ion-exchange and affinity chromatography, the reverse transcriptases of the virus isolated from SU-DHL-1 cells is partially inhibited by antibodies to the reverse transcriptases of C-type viruses of subhuman primate and endogenous feline, but not of murine, origin. Conversely, antibody prepared against the purified SU-DHL-1 viral reverse transcriptase, at concentrations which maximally inhibit the homologous enzyme, partially inhibits the reverse transcriptases of subhuman primate C-type viruses, but has little or no inhibitory activity against the reverse transcriptases of feline or murine leukemia viruses. The viruses produced by the SU-DHL-1 and SU-AmB-3 cell lines have been shown to be infectious for normal human peripheral blood mononuclear cells, normal human bone marrow cells, and certain human lymphoblastoid cell lines. After infection by these viruses, normal human peripheral blood mononuclear cells and human bone marrow cells have exhibited striking changes in growth behavior and morphology which, though not permanently sustained, have many of the features of abortive transformation.
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PMID:Biology and virology of the human malignant lymphomas: 1st Milford D. Schulz Lecture. 8 2

A foamy virus present in human nasopharyngeal carcinoma tissue was studied for a number of biological properties, including range of cellular susceptibility, growth curve, evolution of cytopathic effect in relation to cellular fusion and intracellular viral distribution, reverse transcriptase activity, and buoyant density. The virus was also studied immunologically and found to be closely related to the chimpanzee foamy viruses, particularly simian foamy virus type 6, with which it shares common antigens in complement-fixing, fluorescent, and neutralizing antibody tests. In view of this close immunological relationship and the failure to find antibody to the human isolate in sera from more than 250 humans, including 50 patients with nasopharyngeal carcinoma and Burkitt's lymphoma, it is suggested that the isolate is not a human representative of the foamy virus group but rather a variant strain of chimpanzee foamy virus.
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PMID:Human foamy virus: further characterization, seroepidemiology, and relationship to chimpanzee foamy viruses. 20 31

Velocity sedimentation of uridine-labelled cultures was found to be more reliable than isopycnic sedimentation in detecting oncornavirus production in lymphoid cells. Of 13 cell lines (including six derivea from Burkitt's lymphomas and two from leukaemic leukocytes) only one, the leukaemia-derived, Epstein-Barr virus-producing line QIMR-WIL, showed any activity. The nature of the QIMR-WIL particles was further defined by isolation of uridine-labelled 70S RNA and by the simultaneous assay for reverse transcriptase and 70S RNA, but production of such particles was detected in only three of 10 assays. Pretreatment of cells with 5'-iododeoxyuridine or culture in arginine-free medium did not induce particle production. Syncytia assays using XC cells were negative. Of 13 primary cultures (nine samples of leukaemic leukocytes and four of cord leukocytes) treated with mitogens and subjected to inducing conditions, one (leukocytes from a patient with acute myelogenous leukaemia) showed evidence in successive assays of oncornavirus synthesis. The low and transient yield of oncornavirus-like particles obtained in this work parallels that reported in previous studies of fresh lymphoid cells and primary cultures.
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PMID:Survey of human lymphoblastoid cell lines and primary cultures of normal and leukaemic leukocytes for oncornavirus production. 97 88

The secretion of insulin-like growth-factor-binding proteins (IGFBPs) and expression of the genes encoding IGFBP-1, IGFBP-2 and IGFBP-3 have been studied in a panel of cell lines derived from breast carcinomas, Wilms' tumour, neuroblastoma, retinoblastoma, colon carcinoma, liver adenocarcinoma, Burkitt's lymphoma and a non-small-cell lung carcinoma. All cell lines, with the exception of the Burkitt's lymphoma cell line, secreted IGFBPs, as detected by affinity labelling. A 34-kDa BP was present in the conditioned media of all IGFBP-secreting cell lines, whereas BPs ranging from 18 kDa to 53 kDa were variably secreted. All IGFBP-secreting cell lines expressed the IGFBP-2 gene as determined by Northern blot analysis. The Wilms' tumour, the neuroblastoma and the retinoblastoma cell line expressed the IGFBP-2 gene only. All other cell lines, with the exception of the Burkitt's lymphoma, expressed the IGFBP-2 gene and, in addition, either the IGFBP-1 gene and/or the IGFBP-3 gene. IGFBP-1 gene expression could be detected by reverse transcriptase polymerase chain reaction only. IGFBP-3 gene expression was detected by Northern blot analysis, but transcripts were less abundant than IGFBP-2 mRNAs. These findings indicate that the expression of multiple BP genes and the secretion of BPs may be a common property of tumour cells.
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PMID:Insulin-like growth-factor-binding protein gene expression and protein production by human tumour cell lines. 137 87

Burkitt's lymphomas, linked by previous studies with the DNA-containing Epstein-Barr virus, contain an RNA related in sequence to that of Rauscher leukemia virus. The present study establishes that the viral-related RNA found in Burkitt's tumors is a 70S component encapsulated with RNA-instructed DNA polymerase in a particle possessing a density characteristic of RNA tumor viruses. Further, the DNA synthesized by the Burkitt particles hybridizes specifically to the RNA of Rauscher leukemia virus. Thus, four features characteristic of a known oncogenic RNA agent are also exhibited by particles found with a high (87%) frequency in Burkitt's tumors. The relation between the RNA particle and the Epstein-Barr virus and their etiological roles remains to be elucidated. However, relevant to these issues is the finding reported here that the presence of Epstein-Barr virus information in nonneoplastic cells does not lead to the production of the RNA particles that have been detected now in three different human neoplasias, including leukemias, breast cancer, and Burkitt's disease.
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PMID:Burkitt's tumors contain particles encapsulating RNA-instructed DNA polymerase and high molecular weight virus-related RNA. 412 90

Nucleic acid base analogues were used to examine a Herpesvirus saimiri (HVS)-infected marmoset lymphoid cell line (MLC-1) for possible association with type C viruses. Synthetic templates poly(rA).d(pT)(10) and poly(dA).d(pT)(10) were used to detect RNA-directed DNA polymerase activity in 100-fold concentrated tissue culture fluids. HVS was monitored by immunofluorescence for early, late, and membrane antigens. MLC-1 cells were exposed to 30 mug of 5-bromo-2'-deoxyuridine (BUdR) per ml for 24 h and examined daily. Similar experiments used 5-iodo-2'-deoxyuridine (IUdR) (20 mug/ml) for 30 h or IUdR (20 mug/ml) for 3 days followed by 2% dimethyl sulfoxide for 4 days. Results of these experiments failed to show any type C virus-like polymerase; however, HVS expression was greatly stimulated. BUdR and IUdR enhanced expression of HVS-associated antigens five- to sevenfold, with maximal stimulation being observed 3 to 4 days after removal of the analogue. IUdR-dimethyl sulfoxide treatment was generally less effective. Although more cells showed HVS antigens, the treatments did not increase cell-free infectious virus. The data suggest that HVS-infected lymphoid cells can be stimulated to express virus in a manner similar to that of the Epstein-Barr virus in Burkitt's lymphoma cells. No evidence of type C virus was found in stimulated cultures.
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PMID:Stimulation of Herpesvirus saimiri expression in the absence of evidence for type C virus activation in a marmoset lymphoid cell line. 413 95

Burkitt's lymphoma cell line, P3HR-I, was found to secrete virions with properties of known type-C RNA tumor viruses. The viral particles had a buoyant density of 1.16 g/ml in sucrose gradients and contained a high-molecular-weight RNA and an RNA-instructed DNA polymerase. The viral polymerase was active in an endogenous reaction requiring the presence of the four deoxyriboside triphosphates and manganese ions, and was sensitive to RNase. The DNA product of the endogenous reaction specifically hybridized to P3HR-I viral 60 to 70S RNA. Electron microscopic examination of ultrathin sections of P3HR-I cells revealed immature, mature and budding virions typical of type-C retroviridae. Nucleic acid hybridization assays showed no sequence homoblastosis virus, murine oncornaviruses, simian sarcoma virus or RD114 virus.
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PMID:Evidence for type-C retrovirus production by Burkitt's lymphoma-derived cell line. 624 66

A retrovirus designated RPMI 8226V, isolated in 1973 from the human myeloma cell line RPMI 8226 has been characterized by competition radioimmunoassay (RIA) for the major viral structural protein and by nucleic acid hybridization analysis using cDNA of the virus. The virus is highly related to the squirrel monkey type D retrovirus, SMRV. In the homologous RIA using rabbit anti-RPMI 8226V and 125I-labelled p37 of RPMI 8226V, RPMI 8226V and SMRV exhibited competition of 81% and 73% respectively. Similarly, in the homologous system for SMRV p36, these viruses competed 98 and 100%. Reagents made from the type D retrovirus. Mason Pfizer Monkey Virus (MPMV), known to be related but distinct from SMRV, were used in assays designed to detect interspecies determinants of type D retroviruses. In assays using goat anti-MPMVp26 vs SMRV 125I-p36, RPMI 8226V, SMRV and MPMV competed to the same extent (93%). Hybridization analysis of RPMI 8226V cDNA showed significant homology to cellular RNA and DNA of mink, bat, and human cell infected with RPMI 8226V and to DNA or SMRV infected cells but not to uninfected cells or cells infected with other viruses. These results taken together clearly indicate that RPMI 8226V and SMRV are very closely related to each other. The finding of a type D retrovirus in this human myeloma cell line that had been used in EBV studies (the usual source of EBV being the marmoset cell line B95-8) prompted a survey of RPMI 8226V in some human and marmoset cell lines. The assays included the RIA for p36, nucleic acid hybridization using cDNA of RPMI 8226V, reverse transcriptase analysis and electron microscopy (EM). The results clearly show that in addition to RPMI 8226, human Burkitt lymphoma cells BJAB/B-95-8/K which were supertransformed by EBV from B-95-8/K marmoset cells as well as marmoset cell lines [(B-95-8/K and B-95-8/N) obtained from Stockholm and Uppsala, Sweden] were positive for the RPMI 8226V. Similar lines obtained elsewhere were negative. The results obtained clearly indicate that RPMI 8226V is a serious laboratory contamination in some widely used human cell lines. The possible impact of this viral contamination for some virological and cell biological studies is discussed.
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PMID:Identification of the RPMI 8226 retrovirus and its dissemination as a significant contaminant of some widely used human and marmoset cell lines. 628 81

The expression of the granulocyte colony-stimulating factor (G-CSF) receptor in childhood Burkitt's lymphoma (BL) cells, and the mitogenic effect of G-CSF on these cells, was studied in a panel of 13 Epstein-Barr virus (EBV) positive and negative BL cell lines derived from nine children. G-CSF receptor mRNA expression was investigated by Northern blot analysis and reverse transcriptase polymerase chain reaction (RT-PCR). Binding of G-CSF to BL cell lines was measured by chemical crosslinking of 125I-G-CSF, and proliferation by thymidine incorporation. Inducibility of the G-CSF receptor was studied by stimulation with interleukin-1 beta, tumour necrosis factor-alpha, Staphylococcus aureus Cowan A, anti-human IgM, phorbol myristate acetate, calcium ionophore A23187, and by infection in vitro by immortalizing and non-immortalizing strains of EBV. BL cell lines, unstimulated or stimulated by biological reagents or EBV infection, did not bind radioionated G-CSF in crosslinking experiments. No stimulation by recombinant human G-CSF was observed in 3H-thymidine incorporation assays. No G-CSF receptor mRNA was detected by Northern blot analysis or RT-PCR in BL cell lines. It is concluded that G-CSF plays no direct stimulatory role in the growth of these malignant B-cells, making a deleterious influence of G-CSF in the clinical treatment situation unlikely.
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PMID:Absence of G-CSF receptors and absent response to G-CSF in childhood Burkitt's lymphoma and B-ALL cells. 753 24

Interleukin 10 (IL-10) is a strong B-cell-activating factor. Since murine Ly1-positive peritoneal or lymphoma B cells strongly express IL-10, we examined malignant cells from patients with acute and chronic leukemias by reverse transcriptase polymerase chain reaction (RT-PCR) for the expression of IL-10 mRNA. High expression was found in three out of four samples from CD10+, CD5- common acute lymphoblastic leukemia (cALL) cells, whereas T-ALL samples generally did not contain IL-10 mRNA. In contrast to the murine system, only low levels of IL-10 expression were seen in 10 out of 11 samples from patients with CD5+ CLL. Myeloid derived cell lines were negative for IL-10. Epstein Barr virus (EBV) positive and negative Burkitt's lymphoma (BL) cell lines showed heterogenous IL-10 expression: BL cell lines with a nonactivated germinal center phenotype (CD10+, CD77+, CD23-, CD30-, CDw70-) expressed little or no IL-10, whereas EBV-positive and negative BL cell lines with an activated phenotype (CD77-, CD23+, CD30+, CDw70+) expressed easily detectable amounts of IL-10 mRNA. The highest expression of IL-10 was found in EBV-immortalized lymphoblastoid cell lines (LCL). Upon superinfection with non-defective EBV, the EBV-negative cell line BL 41 up-regulated IL-10 expression. Thus, in vivo IL-10 expression is not restricted to cells showing a specific (CD5+) phenotype. IL-10 may play an important role in c-ALL. The expression of IL-10 in BL cell lines is correlated to an activated phenotype in vitro and is independent of the EBV carrier status. EBV can induce IL-10 expression.
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PMID:Expression of interleukin 10 in B lymphocytes of different origin. 769 7


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