Leukosis
Mostrando 13-24 de 373 artigos, teses e dissertações.
-
13. Cell killing by avian leukosis viruses.
Infection of chicken cells with a cytopathic avian leukosis virus resulted in the detachment of killed cells from the culture dish. The detached, dead cells contained more unintegrated viral DNA than the attached cells. These results confirm the hypothesis that cell killing after infection with a cytopathic avian leukosis virus is associated with accumulatio
-
14. Lack of Sequence Homology Among RNAs of Avian Leukosis-Sarcoma Viruses, Reticuloendotheliosis Viruses, and Chicken Endogenous RNA-Directed DNA Polymerase Activity
The relatedness of the RNAs of the three avian systems, including six avian leukosis-sarcoma viruses, four reticuloendotheliosis viruses, and the microsome fraction of normal uninfected chicken embryo cells, containing RNA and a DNA polymerase have been studied by nucleic acid hybridization. All six avian leukosis-sarcoma viruses have closely related nucleot
-
15. Component of Strain MC29 Avian Leukosis Virus with the Property of Defectiveness
Three clones of morphologically altered cells (L−MC29) of singular properties were isolated from MC29 (subgroup A) leukosis virus-infected chick embryo cells. Supernatant fluids from cultures of the cloned cells produced no transforming or interfering activity on chick embryo cells susceptible to known avian leukosis-sarcoma viruses. No virus associated wi
-
16. Structural analysis of the genomes of gibbon ape and woolly monkey leukosis viruses.
Infectious retroviruses have been isolated from gibbon apes and a woolly monkey. Previous studies have shown that these isolates share some antigenic determinants and that they exhibit partial nucleic acid homology. To further define the relationships in this group of viruses, we compared the RNAs of the viruses of the woolly monkey-gibbon ape class by two-d
-
17. Infrequent involvement of c-fos in avian leukosis virus-induced nephroblastoma.
To determine whether c-fos is involved in avian leukosis virus-induced nephroblastoma, 28 tumors from chickens were analyzed for novel fos fragments. DNA from 1 of 16 clonal outgrowths (in chicken 6561) contained novel fos-related EcoRI and KpnI fragments which hybridized to both v-fos and viral probes. Oncogenicity tests using filtered 6561 tumor cell homog
-
18. Proposal for Numbering Mutants of Avian Leukosis and Sarcoma Viruses
A system for the numbering of mutants of avian sarcoma and leukosis viruses is proposed.
-
19. Avian leukosis virus infection: analysis of viremia and DNA integration in susceptible and resistant chicken lines.
Avian leukosis viruses induce lymphoid leukosis, a lymphoma which develops within the bursa of Fabricius several months after virus infection. Chickens from the Hyline SC and FP lines are, respectively, susceptible and resistant to avian leukosis virus-induced lymphoid leukosis. We examined plasma and cellular DNA obtained from avian leukosis virus-infected
-
20. Genetic determinants of neoplastic diseases induced by a subgroup F avian leukosis virus.
Two subgroup F avian leukosis viruses, ring-necked pheasant virus (RPV) and RAV-61, were previously shown to induce a high incidence of a fatal proliferative disorder in the lungs of infected chickens. These lung lesions, termed angiosarcomas, appear rapidly (4 to 5 weeks after infection), show no evidence of proto-oncogene activation by proviral integration
-
21. Immunological phenotype of lymphomas induced by avian leukosis viruses.
The production of immunoglobulin by six cell lines derived from bursal tumors induced by avian leukosis virus follows two general patterns: (i) three cell lines that have been extensively passaged in culture synthesize and secrete light chains only; (ii) three cell lines that are recently isolated produce and secrete monomeric immunoglobulin M in addition to
-
22. Absence of missense mutations in activated c-myc genes in avian leukosis virus-induced B-cell lymphomas.
We have determined the nucleotide sequences of two independent DNA clones which contained the activated c-myc genes from avian leukosis virus-induced B-cell lymphomas. Neither of these c-myc genes contained missense mutations. This strongly supports the notion that the c-myc proto-oncogene in avian leukosis virus-induced B-cell lymphomas can be oncogenically
-
23. Correlation between cell killing and massive second-round superinfection by members of some subgroups of avian leukosis virus.
Avian leukosis viruses of subgroups B, D, and F are cytopathic for chicken cells, whereas viruses of subgroups A, C, and E are not. The amounts of unintegrated linear viral DNA in cells at different times after infection with cytopathic or noncytopathic viruses were determined by hybridization and transfection assays. Shortly after infection, there is a tran
-
24. On the mechanism of retrovirus-induced avian lymphoid leukosis: deletion and integration of the proviruses.
There is considerable evidence that infection by avian lymphoid leukosis viruses can led to tumor development in the target organ of the host. The mechanism by which virus-induced oncogenic transformation occurs, however, is not clearly understood. As a first step toward deciphering this process, we have characterized the proviruses of the lymphoid leukosis