Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sufficient quantities of human leukocyte interferon have become available for small-scale clinical studies during the past years. The present status of the interferon treatment of respiratory infections, herpes keratitis, hepatitis B, osteogenic sarcoma, and some other tumours is surveyed. The pharmaco-kinetic and toxicological data obtained are summarized. The first clinical experiments with human fibroblast interferon have also been started. The prospects for mass production of human interferons for clinical use are discussed briefly.
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PMID:Prospects for the clinical use of exogenous interferon. 19 14

Nine osteosarcoma cell lines, originally developed from six osteosarcoma tumours in five patients, and two cell lines of non-tumour origin (glia and fibroblast) were grown in vitro in the presence of human leukocyte interferon (L-IF). L-IF exerted a dose-dependent inhibition of growth in all these lines. The inhibitory activity displayed characteristics typical of interferons. Inhibition of cell growth occurred at a much lower L-IF concentration for the osteosarcoma than for the non-tumour-derived lines. Inhibition of tumour cell growth was observed at concentrations obtained in the serum of osteosarcoma patients treated with interferon.
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PMID:Effect of human leukocyte interferon on the growth of human osteosarcoma cells in tissue culture. 26 97

The growth inhibitory effect of human leukocyte and fibroblast interferons was tested in vitro. The effect of fibroblast interferon was more pronounced on osteosarcoma cells and the effect of leukocyte interferon was more pronounced on lymphoid cells. This suggests that the capacity of interferon to inhibit cell growth is, in some measure, tissue specific.
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PMID:Is interferon tissue specific?- Effect of human leukocyte and fibroblast interferons on the growth of lymphoblastoid and osteosarcoma cell lines. 26 37

Murine interferon inhibited the growth of a continuous line of osteogenic sarcoma (OGS) cells in tissue culture. Inhibition of tumor cell growth by interferon was demonstrated by: a) decreased colony formation in soft agar, b) suppression of clone formation in liquid medium, and c) reduction of tumor cell counts in monolayer cultures. This inhibition of cell growth was further documented by suppression of [3H]thymidine uptake by OGS cells exposed to interferon, which suggested inhibition of DNA synthesis of tumor cells. Exposure of tumor cells for 4 hours, 24 hours, and 2,3,4,6, and 8 days demonstrated greater activity with prolonged exposure to interferon. Inhibition of cell growth was significantly greater for OGS cells than for normal mouse embryo fibroblasts. Finally, the antitumor activity of the interferon preparation could be reversed by anti-interferon antibody.
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PMID:Antitumor activity of interferon against murine osteogenic sarcoma cells in vitro. 27 70

A consecutive series of osteosarcoma patients from one hospital is described. In 1962 radiotherapy with delayed surgery according to Cade was replacing surgery alone as the adopted treatment programme. Statistically the results were the same before and after this time with 5 out of 29 and 6 out of 21 patients, respectively, surviving 5 years. With radiation alone none out of eight survived. Surgery alone produced 3 out of 14 and radiation with delayed surgery 6 survivors out of 15. As surgery with or without radiotherapy is equally ineffective in controlling osteosarcoma a prospective randomized trial of the relative merits of chemotherapy and interferon as adjuvant therapy seems highly desirable.
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PMID:Radiotherapy and surgery in 50 cases of osteosarcoma treated without adjuvant chemotherapy. 27 13

Interferon was used to treat C57BL/6 female mice inoculated with a continuous line of murine osteogenic sarcoma cells. A short 7-day course of 30,000--60,000 U/day of tpe I interferon either completely inhibited or delayed the appearance of tumors in experimental animals. The therapeutic efficacy of type I interferon was compared with murine serum that contained type II interferon as well as other lymphokine activity. Tumor development was strikingly inhibited in animals treated for 7 days with serum containing only 600 U of type II interferon. Inhibition of tumor development was thus achieved with 100-fold less interferon than that required with type I preparation.
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PMID:Inhibition of murine osteogenic sarcomas by treatment with type I or type II interferon. 27 65

Murine interferon inhibited the growth of a continuous line of osteogenic sarcoma cells in tissue culture. Inhibition of tumor cell growth was documented by decreased clone formation in liquid medium, decreased tumor cell counts in monolayer cultures, suppression of colony formation in semi-solid agar, and decreased uptake of 3H-thymidine by the osteogenic sarcoma cells in culture. The capacity of anti-interferon antibody to block the tumor cell growth inhibitory activity of the interferon preparation suggested that interferon itself is the biologically active component of the interferon preparations. In vivo, a 7-day course of 30,000-60,000 units/day of type I interferon prepared in cell cultures either completely inhibited or delayed the appearance of tumors in experimental animals inoculated with osteogenic sarcoma cells by the sc route. The therapeutic efficacy of a preparation of murine sera containing type II interferon as well as other lymphokine activity was compared with the type I interferon preparation. Animals treated with 600 units of type II interferon were protected against tumor development as effectively as with 60,000 units/day of type I.
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PMID:Antitumor activity of interferon against murine osteogenic sarcoma in vitro and in vivo. 28 6

Twenty-nine patients, 27 of them with osteosarcoma and two with juvenile laryngeal papilloma, were followed for an aggregate period of 365 months, during which time they received long-term treatment with human leukocyte interferon. The interferon was given by intramuscular injection either daily or three times a week; the dose was 3 x 10(6) standard units. During the course of the treatment, 12 distinct symptoms were recognized as possible side effects of the drug; the three most frequent symptoms occurring after injection were fever, local pain, and shivering. All but three of the patients reported between one and five symptoms. Partial purification of the interferon reduced or eliminated some, but not all, of the symptoms. All of the patients were treated on an ambulatory basis, and none had to discontinue the interferon therapy because of the side effects.
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PMID:Side effects of long-term treatment with human leukocyte interferon. 29 35

Peripheral lymphocytes from patients with osteosarcoma receiving interferon (IF) as adjuvant therapy were tested in vitro for response to various mitogens. Prolonged parenteral administration of IF preparations caused no major change of the mitogen responses. The ability of IF, when added in vitro, to inhibit lymphocyte response to mitogens was not altered to any major extent by in vivo administration of IF.
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PMID:Effect of prolonged in vivo administration of leukocyte interferon on the mitogen responsiveness of human lymphocytes. 29 28

The production of a cytotoxic factor synthesized by human haemic killer cells growing in vitro is described. The factor can be found extra- and intra-cellularly. It is released from the cells by an apocrine form of secretion, illustrated by light and electron micrographs. The culture fluid from 14C-labelled killer cells reveals numerous radioactive bands following SDS-gel electrophoresis. The killing factor is precipitated by 30 to 60% saturation of ammonium sulphate. Cultures of human rhabdomyosarcoma and osteosarcoma cells are more susceptible to the killer cells than normal human dermal or lung fibroblasts. During contact or killer with target cells a higher level of cytotoxic activity can be detected in the culture fluid. The cell-killing activity is completely inactivated by 30 min at 60 degrees C, but it is not absorbed by target cells during 1 h of incubation. The cytotoxic factor is unlikely to be an interferon since it did not prevent the replication of a wide range of viruses and only a low level of interferon could be detected in the culture medium. The introduction of Strep. faecalis into cultures of killer cells caused their transformation into immunoblast-like cells, indicating their lymphoid origin. The cells did not phagocytose the microorganism. When the humoral factor was injected into fibro-sarcoma-bearing mice approximately 50% survived, whereas all control animals died.
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PMID:A humoral cytotoxic substance produced by a human killer cell line. 41 8


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