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Biomedical subjects

J Smida

Publications and source records attributed to J Smida.

At least 37 records · Page 2Linked to original sources
PubMed1983

Metastasizing fibrosarcomas in hamsters (BMH) after injection of B77 sarcoma virus transformed mouse cells.

Injection of virogenic mouse cells B77-1026 into newborn Syrian hamsters resulted in arising of progressively growing autochthonous fibrosarcomas. From hamster tumors five stable tumor cell lines (BMH/1--BMH/5) were established in vitro. All cells of the newly established tumor cell lines had hamster karyotype, they were able to grow in soft agar and did not contain rescuable B77 viral genome. BMH tumor cells injected into syngeneic newborn as well as young adult hamsters produced tumors at the site of application and metastasized frequently into viscera. From metastases in different organs further tumor cell lines and single cell clones were established in vitro. All these tumor cell lines and clones exhibited higher metastatic capacity than the parent cell lines.

Animals↗
PubMed1980

Isolates of avian sarcoma virus Bratislava 77 (B77) oncogenic for mammals do not contain an excess of transformation-defective mutants.

Several isolates of the avian sarcoma virus Bratislava 77 (B77), used in tumor induction in rats, hamsters and mice, were tested for the excess of spontaneously segregated transformation-defective mutants (tdB77). The question was asked whether these td mutants could interfere with transforming sarcoma viruses at tumor induction in mammals. It was found that the B77 virus isolates used in successful sarcoma induction in mammals did not contain an excess of td mutants. One virus isolate which had an excess of td mutants did not induce tumors in mammals. The further characterization of the rescued viruses from virogenic mammalian cells showed that all rescued viruses had the same sub-group C specificity as the original isolate of B77 virus. The integration of the viral genome into mammalian cellular genome did not alter transforming ability of the rescued viruses on duck embryo cells. It seems that propagation of B77 virus in conditions in vivo did not support the segregation, and accumulation of an large excess of td mutants in stocks of B77 virus.

Animals↗
PubMed1979

Heterogeneity of neoplastic cells derived from a hamster tumor induced by avian sarcoma virus B77.

Cells derived from a hamster tumor induced by avian sarcoma virus Bratislava 77 (B77) in vivo, were cultivated in vitro. After few passages two morphologically different cell lines were isolated from the parental culture (B77/H). One cell line consisted of fibroblastic cells (B77/H/fi and the other from epithelioid cells (B77/H/ep). Cells of both lines were highly tumorigenic in neonatal syngeneic hamsters, B77/H/ep cells were able to form colonies in soft agar and contained complete integrated B77 viral genome. In contrast, the B77/H/fi cells grew poorly in soft agar and did not contained B77 virus genome.

Animals↗
PubMed1978

Increased pathogenicity of avian sarcoma virus B77 in cyclophosphamide treated chickens.

The course of sarcoma development was studied in cyclophosphamide treated and control chickens injected with avian sarcoma virus B77 (B77V). It was found that the incidence of sarcomas was the same for both groups of birds. Progressive growth of sarcomas as well as high tumor mortality was observed in drug treated birds, whereas frequent regressions occurred in controls. The drug treatment after B77V infection did not change the response patterns and no cytostatic effect of the drug was observed. Cyclophosphamide treatment improved the rescuability of B77V genome from the transformed virogenic mouse and rat cells in vivo.

Animals↗
PubMed1977

Cyclophosphamide induced sensitivity against avian RNA myeloblastosis virus in age-resistant hosts.

The effect of cyclophosphamide administration on survival of 4- to 7-week-old chickens as well as on induction of leukemia after avian myeloblastosis virus (AMV) injection was studied. The drug treatment alone did not cause any neoplastic effect in the birds during 4 months of observation. Immediate application of AMV to cyclophosphamide-pretreated age-resistant chickens induced acute myeloblastic leukemia in about 80 per cent of test animals. The sensitivity of chickens against AMV, induced by cyclophosphamide, had transient character only. When AMV was injected delayed, 3 or 10 days later, after the administration of the drug was completed, a rapid and pronounced increase of resistance was observed again.

Aging↗
PubMed1976

Nonspecific immunosuppression and expression of avian myeloblastosis virus (BAI strain A).

Chickens were treated with cyclophosphamide in order to induce nonspecific immunosuppression. Treated and untreated animals were injected with avian myeloblastosis virus (AMV) or myeloblasts at the age when a pronounced resistance to the disease is observed. Chickens treated with cyclophosphamide and then challenged with AMV developed acute myeloblastic leukemia in 70 percent. Similarly treated chickens transplanted with fresh AMV producing myeloblasts exhibited 30 percent incidence of myeloblastosis. In contrast, the control animals without treatment showed no myeloblastosis either after myeloblasts application or AMV injection. These results have shown that nonspecific immunosuppression by cyclophosphamide treatment strongly affects the expression of AMV in age-resistant chickens.

Adenosine Triphosphatases↗
PubMed1975

A cell-free mammalian protein-synthesizing system stimulated by RNA from avian myeloblastosis virus.

Carcinoma cells, oncornavirus-infected cells and fetal bovine tissue provide salt wash ribosomal factors capable of responding to avian myeloblastosis virus (AM virus)-RNA and stimulating the incorporation of amino acids into proteins as well as catalyzing the binding of N-acetylated (35S) methionyl-tRNA. The exogenously dependent amino acid incorporation system is stimulated by the high molecular weight species of AM virus-RNA only, particularly the fraction containing polyadenylate (poly(A)) residues; the system is also markedly inhibited by the low molecular weight AM virus-RNA species. Activity for the exogenous system displays very definite divalent/monovalent cation optima and requires the presence of mammalian transfer RNA.

Animals↗
PubMed1975

Neoplastic transformation of mouse embryo cells by virus released from tumorigenic mouse cells transformed by avian sarcoma virus B77.

Mouse C3H embryo cells were transformed in vitro by avian sarcoma virus Bratislava 77 (B77) released scantily from a mouse cell line transformed earlier by the same virus. B77 virus transformed C3H embryo cells contained B77 viral genome and were transplantable into syngeneic as well as allogeneic DBA/2J young mice in which autochthonous sarcomas were induced. Tumors in both strains of mice were virogenic. The probable reasons for an increased transformation capacity of B77 virus in mammals are discussed.

Animals↗