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)

A 40 year old woman with Hodgkin's disease twice developed signs of encephalitis while being treated with prednisone and cyclophosphamide for 10 months. Since on both occasions her Toxoplasma dye test titer was 1 : 8000 or higher, she was treated on suspicion of toxoplasmosis with sulfadizine and pyrimethamine. Her tumor therapy was changed to bleomycin with lower doses of prednisone for 12 months. After death from central pontine myelinolysis, Toxoplasma and cytomegalovirus could be isolated, but no lesions attributable to these infectious agents were present. Maintenance of the patient's immune competence suggested an inquiry into the effects of the chemotherapeutic agents and of tumor infiltration for their respective interference with immunity. Using hamsters with chronic latent toxoplasmosis, it was found that both cortisone and cyclophosphamide caused recrudescence of chronic inapparent infection, that vinblastine and bleomycin interfered only slightly with the development of immunity, whereas in infiltrating lymphoma permitted immunity to develop normally. It is concluded that greater attention should be directed to the immunosuppressive effects of tumor treatment. By choice of an effective tumor therapy which is least immunosuppressive, and if necessary under cover of antimicrobial therapy, a patient with Hodgkin's disease can be aided in developing immunities which he may subsequently be able to maintain.
Infection 1978
PMID:Immune competence in a patient with Hodgkin's disease and relapsing toxoplasmosis. 7 57

Humoral antibodies can be induced in cotton topped (CT) marmosets with killed Herpesvirus saimiri (HVS) vaccines. The serum antibodies delayed, but did not prevent, malignant lymphoma in actively and passively immunized monkeys after inoculation with 10(3.8)TCID50 of cell-free HVS. Experiments are in progress to determine whether the vaccines are able to protect against smaller challenge dosages of HVS. The immunized monkeys were not resistant against transplantation of tumor cells. Infection with Epstein-Barr virus (EBV) and Marek's disease virus (MDV) did not protect against the tumors caused by superinfection with HVS. Attenuation of HVS was not achieved by passaging the HVS genome through different monkey species.
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PMID:Experiments to vaccinate marmoset monkeys against malignant lymphoma. 16 14

Infection of Moloney mouse sarcoma virus (M-MSV) in adult mice of several inbred strains revealed that all strains except AKR are highly susceptible to M-MSV tumor development. F1 hybrids between AKR and CBA, DBA/2 or NIH mice are as resistant (93%) as the parental AKR strain, which indicates that resistance is transmitted as a dominant character. First backcross mice to the susceptible parent show a 3:1 ratio of resistant to susceptible mice. This is the expected ratio for two segregating loci which independently confer resistance. The incidence of resistant F2 mice is somewhat lower than expected. Further support for the two-gene hypothesis was obtained in second backcross mice. None of the major genes affecting MuLV infection (Fv-2 and H-2) seems to play any role in this system and no linkage was found with Thy. 1 and albino, dilute, agouti and brown markers.
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PMID:Genetic control of oncogenesis by murine sarcoma virus Moloney pseudotype. I. Genetics of resistance in AKR mice. 17 Feb 19

Infection of herpes simplex virus type-2-transformed hamster tumor cells with adeno-associated virus type 1 before inoculation into hamsters specifically delayed the appearance of palpable tumors and increased the survival time of the animals. The data indicated that a defective virus of humans can influence cancer expression by a virus-transformed cell.
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PMID:Effect of adeno-associated virus on cancer expression by herpesvirus-transformed hamster cells. 17 33

Infection with Marek's disease virus (MDV) and subsequent tumor development failed to induce the expression of endogenous avian RNA tumor virus genome in Line-15I and Line-7 chickens which lacked such expression at 1 day of age. Titers of avian leukosis virus (ALV) group-specific (gs) antigen detected by the COFAL test and expression of chick helper factor (chf) activity remained relatively constant in birds which expressed these genome functions at hatching time. Endogenous ALV belonging to the E-subgroup was isolated from two of 50 birds; both were controls not exposed to MDV. There was no correlation between expression of ALV genome (gs or chf) at 1 day of age and the rate of tumor development subsequent ot MDV infection. It was concluded that MDV infection can induce tumors without the participation of endogenous ALV genome.
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PMID:Lack of correlation between Marena tumor induction and expression of endogenous avian RNA tumor virus genome. 17 29

Previous reports described the induction of avian renal neoplasms by leukosis virus strains BAI A [avian myeloblastosis virus (AMV)] and MC29, and illustrated morphological characteristics of the tumors. Continued studies in this work confirm evidence of the origin of the tumors from embryonal cells residual in the posthatched chick. The work further emphasizes differences in histopathology of the neoplasms caused by the two viruses and reveals differences in the histopathogenesis of the respective growths. Embryonal rests may consist of two types of cells, those of epithelial characteristics and a second element of differentiation between nephroblastema (mesenchyme) and epithelium and designated here as nephromesoblastoma. Infection by AMV induces tumors of epithelial characteristics and, in addition, derivatives of nephromesoblastoma consisting of cartilage, bone, areas of keratinization, and sarcoma. Keratinized structures in the nephroblastoma originate from nephromesoblastoma. In contrast, MC29 virus induces only epithelial growths representing principally aberrant and malformed glomerular and tubular structures with occasional cartilage derived from epithelial cells. MC29 tumors are completely lacking in nephromesoblastoma tissue and contain no bone, sarcoma, or keratinized formations. In MC29 tumors, occasional cartilage was derived from epithelium. Tumors caused by AMV exhibit the complex structure of nephroblastoma with all of the features of the growth in humans (Wilms' tumor). The neoplasms induced by both AMV and MC29 exhibit marked aberration, distortion, and malformation in the differentiation of the cells growing out from the embryonal rests representing rare manifestations of cell genetic influence inherent in the primordial growth of nephroblastema. The results thus illustrate fundamental differences in cellular composition and capacity to respond to etiologically different leukosis viruses.
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PMID:Renal neoplastic response to leukosis virus strains BAI A (avian myeloblastosis virus) and MC29. 17 94

To see if integration of the provirus resulting from RNA tumor virus infection is limited to specific sites in the cell DNA, the variation in the number of copies of virus-specific DNA produced and integrated in chicken embryo fibroblasts after RAV-2 infection with different multiplicities has been determined at short times, long times, and several transfers after infection. The number of copies of viral DNA in cells was determined by initial hybridization kinetics of single-stranded viral complementary DNA with a moderate excess of cell DNA. The approach took into account the different sizes of cell DNA and complementary DNA in the hybridization mixture. It was found that uninfected chicken embryo fibroblasts have approximately seven copies, part haploid genome of DNA sequences homologous to part of the Rous-association virus 2 (RAV-2) genome. Infection with RAV-2 adds additional copies, and different sequences, of RAV -2- specific DNA. By 13 h postinfection, there are 3 to 10 additional copies per haploid genome. This number can not be increased by increasing the multiplicity of infection, and stays relatively constant up to 20 h postinfection, when some of the additional viral DNA is integrated. Between 20 and 40 h postinfection, the cells accumulated up to 100 copies per haploid genome of viral DNA. Most of these are unintegrated. This number decreases with cell transfer, until cells are left with one to three copies of additional viral DNA sequences per haploid genome, of which most are integrated. The finding that viral infection causes the permanent addition of one to three copies of integrated viral DNA, despite the cells being confronted with up to 100 copies per haploid genome after infection, is consistent with a hypothesis that chicken cells contain a limited number of specific integration sites for the oncornavirus genome.
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PMID:Synethesis and integration of viral DNA in chicken cells at different time after infection with various multiplicities of avian oncornavirus. 17 85

A new class of linear duplex DNA structures that contain simian virus 40 (SV40) DNA sequences and that are replicated during productive infection of cells with SV40 is described. These structures comprise up to 35% of the radioactively labeled DNA molecules that can be isolated by selective extraction. These molecules represent a unique size class corresponding to the length of an open SV40 DNA molecule (FO III), and they contain a heterogeneous population of DNA sequences either of host or of viral origin, as shown by restriction endonuclease analysis and nucleic acid hybridization. Part of the FO III DNA molecules contain viral-host DNA sequences covalently linked with each other. They start to replicate with the onset of SV40 superhelix replication 1 day after infection. Their rate of synthesis is most pronounced 3 days after infection when superhelix replication is already declining. Furthermore, they cannot be chased into other structures. At least a fraction of these molecules is infectious when administered together with DEAE-dextran to permissive cells. After intracellular circularization, superhelical DNA FO I with an aberrant cleavage pattern accumulates. In addition, tumor and viral capsid antigen are induced, and infectious viral progeny is obtained. Infection of cells with purified SV40 FO I DNA does not result in FO III DNA molecules in the infected cells or in the viral progeny. It is suggested, therefore, that these FO III DNA molecules are perpetuated within SV40 virus pools by encapsidation into pseudovirions.
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PMID:Infectious linear DNA sequences replicating in simian virus 40-infected cells. 18 87

We studied synthesis of viral and cellular RNA in the presence and absence of 5-fluorodeoxyuridine (FdU, an inhibitor of DNA synthesis) during lytic infection with polyoma virus in confluent, primary mouse kidney cell cultures. In the presence of FdU, synthesis of early 19S polyoma mRNA and of polyoma tumor (T)-antigen, i.e. expression of the early viral gene, is rapidly followed by a mitogenic reaction of the host cell; it leads to an increase of 30 +/- 5% in cellular, mainly 28S and 18S rRNA, followed by activation of the cellular DNA-synthesizing apparatus. Polyoma-induced cellular RNA synthesis is paralleled by increased production of early 19S mRNA and begin of expression of the late viral genes, leading to synthesis of small amounts of late 19S and 16S mRNAs. Changed expression of the viral genome occurs in the absence of detectable synthesis of polyoma DNA I. Infection in the absence of FdU induces the same sequence of events; it is followed, however, by duplication of the mouse cell chromatin (S-phase) and production of progeny virus.
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PMID:Polyoma-induced stimulation of cellular RNA synthesis is paralleled by changed expression of the viral genome. 19 91

Cells of the Raji and NC37 lines can be induced by chemical inducers, such as BrdUrd and IdUrd, or the tumor-promoter TPA to EA-expression only, but do not reveal any VCA synthesis. After superinfection by nontransforming P3HR-1 EBV, however, a varying percentage of the cell population shows VCA synthesis and releases infectious viral particles. The recovered virus differs biologically from P3HR-1 EBV since it transforms human umbilical cord blood lymphocytes into EBNA-positive lymphoblastoid cell lines. Cells of these established lines are susceptible to renewed infection by P3HR-1 EBV which results in EA induction and VCA synthesis. Only cells of one line, NC37-R1, spontaneously produce VCA and EBV particles, which reveal transforming properties and do not induce EA upon superinfection of Raji cells. Infection of P3HR-1 EBV-converted BJA-B cells also leads to EA and VCA induction and the release of viral particles. In contrast to particles recovered from Raji and NC37 cells, no transforming activity was detectable in these virus preparations. According to these data, we propose that viral genomes persisting within Raji and NC37 cells are defective and become complemented by the superinfecting P3HR-1 virus.
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PMID:Recovery of transforming EBV from non-producer cells after superinfection with non-transforming P3HR-1 EBV. 21 77


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