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الصفحة 1 من عند 26 النتائج

Intracavitary chemotherapy with activated cyclophosphamides and simultaneous systemic detoxification with protector thiols in Sarcoma 180 ascites tumor.

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Activated cyclophosphamides such as 4-sulfoethylthiocyclophosphamide (mafosfamide) are suitable for a local intracavitary chemotherapy, whereas cyclophosphamide requires a metabolic activation. Mafosfamide administered i.p. in mice was less toxic (50% lethal dose, 640 mg/kg) than its i.v.

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

Increased glutathione peroxidase activity in a human sarcoma cell line with inherent doxorubicin resistance.

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Several mechanisms of drug resistance have been defined using cell lines selected for resistance in vitro. However, the relevance of these to tumor cell resistance in vivo remains unclear. We established tumor cell lines from biopsies of human sarcomas before and after doxorubicin therapy. One

Expression of drug resistance related proteins in sarcomas of the pulmonary artery and poorly differentiated leiomyosarcomas of other origin.

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Sarcomas are known to develop resistance to current chemotherapeutic strategies, displaying a multidrug-resistant phenotype. Mechanisms involved in drug resistance include reduced cellular drug accumulation, drug detoxification as well as alterations in drug target specificity. In seven sarcomas of

An aza-macrocycle containing maltolic side-arms (maltonis) as potential drug against human pediatric sarcomas.

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BACKGROUND Identification of new drugs against paediatric sarcomas represents an urgent clinical need that mainly relies on public investments due to the rarity of these diseases. In this paper we evaluated the in vitro and in vivo efficacy of a new maltol derived molecule (maltonis), belonging to

[Intracavitary chemotherapy of S 180 ascites sarcoma in mice with 4-(S-ethanol)-sulfido-cyclophosphamide in combination with protector thiols].

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The experimental and pharmacokinetic basis for the local chemotherapy of body cavities with 4-(S-ethanol)-sulfido-cyclophosphamide (P1), a stable derivative of activated cyclophosphamide (CP), was evaluated on the S 180 ascites sarcoma in mice. The severe local toxicity of P1 observed after

Possible involvement of stem-like populations with elevated ALDH1 in sarcomas for chemotherapeutic drug resistance.

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Elevated aldehyde dehydrogenase 1 (ALDH1) has been proposed as one of the possible candidates for a stem cell maker that can be used for the isolation of cancer stem cells from cancers such as leukemia and breast cancer. In the current study, we found that subpopulations with elevated ALDH1 were

V-ATPase is a candidate therapeutic target for Ewing sarcoma.

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Suppression of oxidative phosphorylation combined with enhanced aerobic glycolysis and the resulting increased generation of protons are common features of several types of cancer. An efficient mechanism to escape cell death resulting from intracellular acidification is proton pump activation. In

Oxidative stress and therapeutic opportunities: focus on the Ewing's sarcoma family of tumors.

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Reactive oxygen species (ROS) are highly reactive by-products of energy production that can have detrimental as well as beneficial effects. Unchecked, high levels of ROS result in an imbalance of cellular redox state and oxidative stress. High levels of ROS have been detected in most cancers, where

Isolated liver perfusion for liver metastases: pharmacokinetic advantage?

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The pharmacokinetic advantage of a novel system to noninvasively isolate the hepatic venous outflow and infuse high doses of chemotherapy (doxorubicin or 5-FU) is discussed and compared with intravenous infusion and intra-arterial infusion without hepatic venous detoxification. This dose

Protection against tumorigenesis by 3-methylcholanthrene in mice by beta-naphthoflavone as a function of inducibility of methylcholanthrene metabolism.

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The noncarcinogenic enzyme inducer beta-naphthoflavone (beta-NF) causes an increase in both rate of activation and of detoxification of polycyclic aromatic hydrocarbon carcinogens in tissues of mice of induction-responsive strains. An experiment was carried out to test whether pretreatment with

The reaction of Cytembena with cellular thiol compounds.

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Cytembena has been shown to undergo a rapid addition reaction with a number of thiol compounds, including glutathione and cysteine, resulting in alkylation of the sulphur. Administration of Cytembena to Yoshida sarcoma cells and to L1210 leukemia cells resulted in a loss of titratable thiol groups

Thiol manipulation as a means of overcoming drug resistance in a novel cyclophosphamide-induced resistant cell line.

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Acquired drug resistance is a major obstacle in the successful treatment of cancer by chemotherapy. To study mechanisms of resistance to alkylating agents, we have derived an in vitro subline of the murine KHT-iv sarcoma, KHT-rcp/iv, that has acquired resistance to cyclophosphamide. Compared to the

Protection of hydroquinone-induced apoptosis by downregulation of Fau is mediated by NQO1.

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The Fau gene (Finkel-Biskis-Reilly murine sarcoma virus (FBR-MuSV)-associated ubiquitously expressed gene) was identified as a potential tumor suppressor gene using a forward genetics approach. Downregulation of Fau by overexpression of its reverse sequence has been shown to inhibit apoptosis

Molecular genetics and cellular events of K-Ras-driven tumorigenesis.

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Cellular transformation and the accumulation of genomic instability are the two key events required for tumorigenesis. K-Ras (Kirsten-rat sarcoma viral oncogene homolog) is a prominent oncogene that has been proven to drive tumorigenesis. K-Ras also modulates numerous genetic regulatory mechanisms

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