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[Preliminary report of combination chemotherapy including Arsenic trioxide for stage III osteosarcoma and Ewing sarcoma].

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OBJECTIVE To determine the efficacy of Arsenic trioxide combined with other chemo agents in patients with metastatic osteosarcoma and Ewing sarcoma. METHODS From December 2002 to June 2005, 32 patients with metastatic osteosarcoma and Ewing sarcoma were treated with chemotherapy comprised Arsenic

Arsenic trioxide inhibits Ewing's sarcoma cell invasiveness by targeting p38(MAPK) and c-Jun N-terminal kinase.

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Ewing's sarcoma is the second most frequent primary malignant bone tumor, mainly affecting children and young adults. The notorious metastatic capability of this tumor aggravates patient mortality and remains a problem to be overcome. We investigated the effect of arsenic trioxide (As₂O₃) on the

Clinically tolerable concentrations of arsenic trioxide induce p53-independent cell death and repress NF-kappa B activation in Ewing sarcoma cells.

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Ewing sarcoma (ES), a highly malignant pediatric tumor, is consistently associated with translocations that fuse the EWS gene with a member of the ETS family gene, most commonly FLI-1. Despite significant advances with multiagent chemotherapy, surgery and radiotherapy, about 40% of ES patients still

Arsenic trioxide potentiates the effectiveness of etoposide in Ewing sarcomas.

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Ewing sarcomas (ES) are rare mesenchymal tumours, most commonly diagnosed in children and adolescents. Arsenic trioxide (ATO) has been shown to efficiently and selectively target leukaemic blasts as well as solid tumour cells. Since multidrug resistance often occurs in recurrent and metastatic ES,

THE EFFECT OF ARSENIC COMPOUNDS ON THE ROUS CHICKEN SARCOMA.

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Arsenic and arsenious acids, cacodylic acid, atoxyl, and neosalvarsan fail to influence markedly the growth of the Rous chicken sarcoma.

Evaluation of arsenic trioxide by the pediatric preclinical testing program with a focus on Ewing sarcoma.

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Arsenic trioxide was tested against the PPTP in vitro panel (1.0 nM to 10 µM) and against the PPTP Ewing sarcoma in vivo panel administered intraperitoneally at a dose of 2.5 mg/kg daily × 5 per week for a planned treatment duration of 3 weeks. Arsenic trioxide showed a median relative IC(50) value

Arsenic trioxide concentration determines the fate of Ewing's sarcoma family tumors and neuroblastoma cells in vitro.

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Arsenic trioxide (As(2)O(3)) induces both the differentiation and apoptosis of acute promyelocytic leukemia cells in a concentration dependent manner. We assessed the effects of As(2)O(3) in CADO-ES Ewing's sarcoma (ES), JK-GMS peripheral primitive neuroectodermal tumor (PNET), and SH-SY5Y

Interaction of arsenic trioxide and etoposide in Ewing sarcoma cell lines.

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Ewing sarcomas (ES) are highly malignant mesenchymal tumors, which most often occur in children and adolescents. The current treatment of choice comprises wide resection in combination with multimodal chemotherapy including etoposide (Eto). Due to the serious side effects associated with common

Arsenic trioxide induces programmed cell death through stimulation of ER stress and inhibition of the ubiquitin-proteasome system in human sarcoma cells.

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Sarcoma is a rare form of cancer that differs from the much more common carcinomas because it occurs in a distinct type of tissue. Many patients of sarcoma have poor response to chemotherapy and an increased risk for local recurrence. Arsenic trioxide (ATO) is used to treat certain types of

Hemangioendothelial sarcoma of liver from chronic arsenic intoxication by Fowler's solution.

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A Case of Bone Sarcoma Treated by Colloidal Arsenic.

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[Generalized lymphoblastic sarcoma during severe occupational poisoning by arsenic].

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CHANGES IN BONE SARCOMA AFTER INTRAVENOUS INJECTIONS OF A COLLOIDAL SOLUTION OF METALLIC ARSENIC.

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Effect of growth of mouse sarcoma 37 on resistance of mice to semilethal doses of certain trivalent arsenic compounds.

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Case report: Purulent transformation of granulocytic sarcoma: An unusual pattern of differentiation in acute promyelocytic leukemia.

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BACKGROUND Acute promyelocytic leukemia (APL) is a curable subtype of acute myeloid leukemia. APL is currently treated with combination of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) resulting in the induction of apoptosis and differentiation of the leukemic cells. Differentiation

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