Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The retrovirus designated RPMI8226V (isolated from human myeloma cells RPMI8226) has been characterized with respect to its morphological, biochemical and immunological properties as well as its propagation in various animal and human cells. The myeloma cells RPMI8226 produce intracytoplasmatic A-type particles and extracellular particles. The extracellular particles have been classified as immature particles with translucent core center, typical mammalian C-type virus particles and C-type particles with intermediate membrane. However, the budded particles in secondarily infected human neoplastic cells contained complete doughnut-shaped nucleoids. This type of budding is rather characteristic for B-type particles. The 3H-uridine labeled RPMI8226 viral particles have a buoyant density 1.17 g/ml in sucrose gradient containing high molecular weight RNA and the distribution of viral structural proteins in SDS-PAGE is characteristic for oncornaviruses. The internal structural proteins according to MW are ranged from 13 000 to 30 000 daltons. The virus contains a magnesium-dependent reverse transcriptase. The cellular homogenate and viral concentrate from RPMI8226 cultures do not react with antibodies against ALSV, MuLV, FeLV, RD114, MP-MV and SiSLV. The only reaction was scored with anti BLV antibodies. However, anti BLV serum inhibiting the reverse transcriptase activity of BLV to 60% does not cross-react with the reverse transcriptase of RPMI8226V. In contrast to BLV concentrates, neither XC nor KC cells show syncytia formation by RPMI8226V. The RPMI8226V replication is restricted to human tumor and normal human glia-like cells. The possible origin of the virus is discussed.
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PMID:The retrovirus particles in human myeloma cells RPMI8226: morphological, biochemical, immunological and infective transmission studies. 8 Jul 55

Phosphonoacetic acid has been shown to suppress replication of DNA tumor viruses by inhibiting the activity of virus-induced DNA polymerase and consequently viral DNA synthesis. We now have evidence to show that phosphonoacetic acid inhibits also the cellular DNA polymerases alpha, beta, and gamma of L1210 cells as well as reverse transcriptases of two type C viruses. Particularly, the DNA polymerase alpha is just as sensitive as the herpes virus induced DNA polymerase. The DNA polymerases beta and gamma required seven times more phosphonoacetic acid for a 50% inhibition of their activities. Phosphonoacetic acid inhibited the activities of the reverse transcriptase and terminal deoxyribonucleotidyltransferase only at higher concentrations. Kinetic analysis with the DNA polymerase alpha showed that the compound is a non-competitive inhibitor with respect to the substrates and uncompetitive inhibitor with the activated DNA template. Studies on time course of phosphonoacetic acid inhibition revealed that the compound is inhibitory even after the initiation of DNA synthesis. Phosphonoacetic acid also inhibited cell growth as well as the type C virus production; at concentrations above 50 microgram/ml, the inhibitory effect was more profound on the type C virus production than on cell growth.
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PMID:Inhibition of activities of DNA polymerase alpha, beta, gamma, and reverse transcriptase of L1210 cells by phosphonoacetic acid. 8 50

The mouse melanoma B16 contains particles encapsulating a high molecular weight RNA of 60--70S size associated with a reverse transcriptase. The particles possess a density of 1.14--1.18 g/cm3. The RNA shares sequences with the 70S RNAs of several mammalian C-type RNA tumor viruses. The nuclear DNA of the mouse melanoma B16 possesses particle-related sequences not present in the genome of normal C57BL mice.
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PMID:Biochemical studies on RNA tumor virus information and its transmission in B16 murine melanoma. 8 43

Samples of three nonmalignant and seven leukemic human cells were examined for DNA polymerase activity that could be identified as RNA tumor virus reverse transcriptase. Experiments on virus-infected model animal cells provided the basis for cell fractionation procedures, and reconstituted systems of known virus, added to human cells, established a threshold of virus detection by enzyme assay at 1 to 10 particles/cell. DNA polymerase activity with some properties similar to a reverse transcriptase was detected in some of the human leukemic cells. However, parallel analyses of nonmalignant cells showed sufficient similarities to raise serious questions about the specificity of the criteria. Reverse transcriptase activity has been reported to be present in white blood cells from a proportion of cases of leukemia; however, it is concluded from the present study that the usual enzymatic criteria using synthetic template primers, which were used in most of the studies reported, are not sufficient to identify a DNA polymerase activity as viral reverse transcriptase.
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PMID:Detection of reverse transcriptase activity in human cells. 8 60

Benzophenanthridine alkaloids, fagaronine 4, O-methylfagaronine 5,nitidine 1, allonitidine 3 and methoxydihydronitidine 2 have been shown to possess inhibitory activity against reverse transcriptase of RNA tumor viruses. The enzyme inhibition (50%) by these alkaloids was found in the range of 6-60 microgram per milliliter of the reaction mixture when polynucleotide-oligodeoxynucleotide complexes were used as template primers. The results suggested that the benzophenanthridine alkaloids interacted with the template primers (particularly of the A:T base pairs) and not with the enzyme proteins. Kinetics reaction of the reverse transciptase inhibition showed that the alkaloids stopped the DNA polymerase synthesis instantly, probably by interacting with the template primer.
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PMID:Inhibition of reverse transcriptase activity by benzophenanthridine alkaloids. 8 1

From human mycosis fungoides tumor-derived cell lines, Mycoplasma hyorhinis was isolated. This mycoplasma shared the following characteristics with retroviruses: uptake of 3H-uridine, but not of 3H-thymidine in cell culture; banding at 1.16 g/ml sucrose density and partial shift to retrovirus core density position (approximately equal to 1.24 g/ml) after detergent treatment; incorporation of 3H-TMP into high molecular weight material in standard reverse transcriptase assays with the template-primer poly (A) . (dT)12. On the other hand, the specific reverse transcriptase reaction of retroviruses with poly(A) . (dT)12 and poly(C) . (dG) approximately 16 was almost completely abolished in the presence of the mycoplasma. Thus, M. hyorhinis may interfere with identification and isolation procedures for retroviruses.
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PMID:Simulation and prevention of retrovirus--specific reactions by mycoplasmas. 8 23

An RNA-directed DNA polymerase was purified from a cell line derived from a radiation-induced lymphoma in NIH Swiss mice which produced non-infectious type C virus particles. The enzyme was isolated from a high speed particulate fraction which bands at a density of 1.16--1.19 g/ml in a sucrose gradient, and purified by successive chromatography on DEAE-cellulose, phosphocellulose and hydroxyapatite. The purified DNA polymerase has a molecular weight of 68 000, a pH optimum of 7.5, a KCl optimum of 50 mM, and a Mn2+ optimum of 0.25 mM. It prefers (dT)15 . (A)n to (dT)15 . (dA)n as the primer template and transcribes the poly(C) strand of (dG)15 .(C)n and (dG)15 . (OMeC)n. It transcribes heteropolymeric regions of avian myeloblastosis virus 70 S RNA, and is inhibited by antiserum to Rauscher murine leukemia virus DNA polymerase. Comparison of the properties of DNA polymerase purified from radiation-induced lymphoma cells with the DNA polymerase purified from non-defective murine type C RNA tumor viruses shows that the mouse lymphoma enzyme is both biochemically and immunologically related to murine leukemia virus DNA polymerases.
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PMID:Characterization of an RNA-directed DNA-polymerase from a cell line derived from a radiation-induced lymphoma in mice. 9 May 22

Benzophenanthridine alkaloids, fagaronine 4, O-methylfagaronine 5, nitidine 1, allonitidine 3 and methoxydihydronitidine 2 have been shown to posses inhibitory activity against reverse transcriptase of RNA tumor viruses. The enzyme inhibition (50%) by these alkaloids was found in the range of 6-60 microgram per milliliter of the reaction mixture when polynucleotide-oligodeoxynucleotide complexes were used as template primers. The results suggested that the benzophenanthridine alkaloids interacted with the template primers (particularly of the A:T base pairs) and not with the enzyme proteins. Kinetics reaction of the reverse transciptase inhibition showed that the alkaloids stopped the DNA polymerase synthesis instantly, probably by interacting with the template primer.
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PMID:Inhibition of reverse transcriptase activity by benzophenanthridine alkaloids. 9 65

A RNA-dependent DNA polymerase (RTase) was purified from human osteosarcoma tissue by successive column chromatography of the microsomal fraction on DEAE-cellulose (DE-23 and DE-52) and phosphocellulose. The purified enzyme has a molecular weight of about 68,000, a pH optimum of 8.1, a Mg2+ optimum of 0.8 mM, Mn2+ optimum of 1.0 mM and a KCl optimum of 60 mM. The enzyme transcribes (rA)n . (dT)12, (rC)n . (dG)12-18 and (2-O-methyl C)n . (dG)18, but is unable to transcribe (dA)n . (dT)10. The enzyme has no catalytic activity in the presence of oligodeoxynucleotide initiators alone, indicating the absence of terminal deoxynucleotidyl transferase. The purified enzyme is able to transcribe the heteropolymeric regions of a 70S RNA from R(Mu)LV. The presented data support the presence of a RNA-dependent DNA polymerase in human osteosarcoma tissue with biochemical properties, resembling those of C-type RNA tumor viruses.
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PMID:Purification and biochemical characterization of a virus-specific reverse transcriptase from human osteosarcoma tissue. 9 60

By optimal hormonal treatment the production of exogenously transmitted MMTV can be stimulated in vitro to different degrees, depending on cultivation conditions and origin of tumor cells. Moreover, after appropriate hormonal treatment, endogenous MMTV-Y can be rescued from primary cell cultures derived from dimethyl benzanthracene- and hormone-induced C57BL/10 mouse mammary adenocarcinoma, as determined by reverse transcriptase assay, distribution of 3H-uridine-labelled viral particles, immunofluorescence, and electron microscopy. On the contrary, all attempts to rescue MMTV-Y from cultures derived from urethane-induced C57BL/10 tumors failed. These data indicate that upon syncarcinogenic action of non-viral carcinogenes, estrogen and prolactin, the MMTV-Y genome can be expressed in mammary gland parenchymatous cells, which in turn may result in cell transformation. The full MMTV-Y gene expression occur after appropriate hormonal stimulation of the C57BL/10 mammary cancer cells in vitro.
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PMID:Hormone-responsive genes of the mouse mammary tumor virus. 9 6


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