actinomycin d/ساركومة

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Mechanism of actinomycin D-induced resistance in Ridgway osteogenic sarcoma: an ultrastructural study.

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The ultrastructural appearances of actinomycin D treated sensitive and resistant sublines of Ridgway osteogenic sarcoma (ROS) have been correlated with the suggested mechanism of drug-induced resistance. The resistant subline (designated ROS/ADX/G2) was developed by repeated suboptimal treatment of

A phase II evaluation of methyl CCNU and actinomycin D in the treatment of advanced sarcomas in adults.

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Twenty-nine patients with metastatic sarcoma were treated with a combination of methyl CCNU and actinomycin D. Patients with adequate bone marrow reserve received methyl CCNU 100 mg/m2 orally on day 1 and actinomycin D 0.3 mg/m2/day intravenously for five days. Both drugs were repeated every four

Actinomycin-D-resistant in vitro mouse cell line derived from a methylcholanthrene-induced sarcoma: decrease of malignancy and antigenic characteristics.

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The tumorigenic EPO clonal cell line, derived from a methylcholanthrene-induced murine sarcoma, was exposed to increasing concentrations of actinomycin D and gave rise to a subline, resistant to 0.02 mug of actinomycin D per ml of medium, which was designated EPO/ADj. Drug resistance was accompained

Sensitization of AIDS-Kaposi's sarcoma cells to Apo-2 ligand-induced apoptosis by actinomycin D.

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Kaposi's sarcoma (KS) is the most frequent malignancy associated with HIV infection (AIDS-KS), a complication that leads to high mortality and morbidity. AIDS-KS cells are resistant to killing by chemotherapeutic drugs/NK cells and Fas-induced apoptosis, suggesting that the acquisition of

[Combination chemotherapy with vincristin, actinomycin D, cyclophosphamide and adriamycin in soft-part sarcoma].

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Fifteen patients with soft-part sarcoma were treated with combination chemotherapy consisting of vincristin, actinomycin D, cyclophosphamide and adriamycin (VACA therapy). The cumulative five-year survival rate by the Kaplan-Meier method was about 73%. This VACA therapy was effective for malignant

A preliminary study of cyclophosphamide (NSC-26271), adriamycin (NSC-123127), imidazole carboxamide (NSC-45388), and actinomycin D (NSC-3053) with or without MER-BCG in patients with advanced sarcomas.

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Polychemotherapy for soft tissue sarcomas has been reported to produce response rates ranging from 24--60% (1, 2). Immunotherapy has reportedly prolonged survival after surgery for some tumors and enhanced the effectiveness of chemotherapy (3, 4). This report summarizes our preliminary experience

Metastatic sarcomas: chemotherapy with adriamycin, cyclophosphamide, and methotrexate alternating with actinomycin D, DTIC, and vincristine.

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Two-hundred-thirty-two evaluable patients with metastatic sarcomas received a palliative experimental treatment program consisting of Adriamycin, 60 mg/m2, cyclophosphamide, 600 mg/m2, and methotrexate, 25 mg/m2 intravenously every three weeks for two courses. This program was followed by a

Combination chemotherapy using adriamycin, DTIC, cyclophosphamide, and actinomycin D for advanced soft tissue sarcomas: a randomized comparative trial. A phase III, Southwest Oncology Group Study (7613).

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The term soft tissue sarcoma refers to a large variety of malignant tumors arising in extraskeletal connective tissues that connect, support, and surround discrete anatomic structures. All visceral organs also contain a connective stroma that can undergo malignant transformation. Because of the

Involvement of tumour necrosis factor in monocyte-mediated rapid killing of actinomycin D-pretreated WEHI 164 sarcoma cells.

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Human and murine monocyte-macrophages kill actinomycin D (ActD)-treated WEHI 164 sarcoma cells in a 6-hr 51Cr-release assay (drug-dependent cellular cytotoxicity, DDCC). In this study, we have investigated the cytotoxic activity of human recombinant tumour necrosis factor (hrTNF) against untreated

Improved outlook for Ewing's sarcoma with combination chemotherapy (vincristine, actinomycin D and cyclophosphamide) and radiation therapy.

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Vincristine, actinomycin D, and cyclophosphamide (VAC) were administered to 14 patients with Ewing's sarcoma. The primary tumors were treated with radiation therapy and concurrent chemotherapy. Nine patients had no visible metastases at diagnosis: two died following the development of pulmonary

Alternating administration of adriamycin (NSC-123127) and vincristine (NSC-67574)-actinomycin D (NSC-3053) in advanced sarcomas.

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Fifteen patients with surgically incurable, advanced, and metastatic sarcomas were treated with courses of adriamycin and vincristine-actinomycin D alternating within a 7-week cycle. Three patients had objective partial responses for more than 3 months (liposarcoma, 4 months; fibrous histiocytoma,

Isolated limb perfusion with actinomycin D and TNF-alpha results in improved tumour response in soft-tissue sarcoma-bearing rats but is accompanied by severe local toxicity.

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Previously we demonstrated that addition of Tumour Necrosis Factor-alpha to melphalan or doxorubicin in a so-called isolated limb perfusion results in synergistic antitumour responses of sarcomas in both animal models and patients. Yet, 20 to 30% of the treated tumours do not respond. Therefore

Simultaneous inhibition of mitogen-activated protein kinase and phosphatidylinositol 3-kinase pathways augment the sensitivity to actinomycin D in Ewing sarcoma.

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OBJECTIVE Ewing sarcoma cells, of which over 85% retain chimeric fusion gene EWS/Fli-1, are by and large more resistant to chemotherapeutics compared to nonneoplastic cells. The purpose of this study is to determine the role of EWS/Fli-1 fusion and its downstream targets regarding the cells'

A comparison of adriamycin versus vincristine and adriamycin, and cyclophosphamide versus vincristine, actinomycin-D, and cyclophosphamide for advanced sarcoma.

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This randomized study, conducted by the Eastern cooperative Oncology Group, compared Adriamycin (doxorubicin) (70 mg/m2) versus vincristine (1.4 mg/m2) and Adriamycin (50 mg/m2); and cyclophosphamide (750 mg/m2) versus vincristine (1.4 mg/m2), actinomycin-D (0.4 mg/m2), and cyclophosphamide (750

Vincristine, doxorubicin, cyclophosfamide, actinomycin D, ifosfamide, and etoposide in adult and pediatric patients with nonmetastatic Ewing sarcoma. Final results of a monoinstitutional study.

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OBJECTIVE To investigate a six-drug combination in patients with nonmetastatic Ewing sarcoma, focusing on chemotherapy-induced necrosis and chemotherapy toxicity in adult and pediatric patients. METHODS Alternating cycles of vincristine (1.5 mg/m2), doxorubicin (80 mg/m2) and cyclophosfamide (1200

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