adenosine triphosphate/sarcoma

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Adenosine triphosphate-guanosine 5'-phosphate phosphotransferase. IV. Isozymes in human erythrocytes and Sarcoma 180 ascites cells.

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Adenosine triphosphate-guanosine 5'-phosphate phosphotransferase. II. Inhibition by 6-thioguanosine 5'-phosphate of the enzyme isolated from hog brain and sarcoma 180 ascites cells.

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[Experimental production of sarcoma in mice with administration of reducing saccharides, especially maltose, and some effects of adenosine triphosphate on the sarcomatous proliferation of fibroblast induced by injection of reducing saccharides].

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Glutathione metabolism during Yoshida ascites sarcoma growth.

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Glutathione (GSH) metabolism and protein synthesis were observed over a period of about two weeks in Yoshida ascites sarcoma and intracellular concentration relative to days 7, 10 and 13 assumed as 'markers' of different stages of tumor development. During this period the decrease in rate of cell

Use of 5'-γ-ferrocenyl adenosine triphosphate (Fc-ATP) bioconjugates having poly(ethylene glycol) spacers in kinase-catalyzed phosphorylations.

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The 5'-γ-ferrocenyl adenosine triphosphate (Fc-ATP) bioconjugates (3 and 4), containing the poly(ethylene glycol) spacers, were synthesized and compared to a hydrophobic analogue as co-substrates for the following protein kinases: sarcoma related kinase (Src), cyclin-dependent kinase (CDK), casein

Biochemical and cytotoxic actions of 3,6-dihydroxy-4,5-dimethylphthalaldehyde in sarcoma 180 cells.

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The replication of Sarcoma 180 cells in culture was inhibited by 3,6-dihydroxy-4,5-dimethylphthalaldehyde (HMPA). The inhibition of growth caused by HMPA was evident after treatment of cells with drug for only 15 min. This exposure period caused decreased in (a) cloning efficiency, (b) transport

DNA synthesis inpermeable mouse ascites sarcoma cells.

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DNA synthesis was studied in mouse ascites sarcoma cells using a permeable cell system. The sarcoma was induced by the Schmidt-Ruppin strain of Rous sarcoma virus. The cells were made permeable to nucleoside triphosphates by treatment with a hypotonic buffer containing 10 mM Tris Cl, 4 mM MgCl2, 1

Therapy monitoring in human and canine soft tissue sarcomas using magnetic resonance imaging and spectroscopy.

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OBJECTIVE The goals of this study were to determine whether magnetic resonance parameters (a) can identify early during therapy those patients most likely to respond to hyperthermia and radiotherapy, (b) can provide prior to or early during therapy information about the temperature distributions

Involvement of caspase 8 in apoptosis induced by ultrasound-activated hematoporphyrin in sarcoma 180 cells in vitro.

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OBJECTIVE Sonodynamic therapy (SDT), a novel and promising cancer therapy that uses a combination of ultrasound and hematoporphyrin, can induce apoptosis in some cancer cells. However, the mechanism(s) of SDT-induced cell apoptosis is not well understood. This study investigated SDT-induced

On chip electrochemical detection of sarcoma protein kinase and HIV-1 reverse transcriptase.

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In this study, we report a new multiplexed microchip platform exploiting a peptide-modified gold surface and a labeled electrochemical approach. The significance of the presented methodology lies in its ability to test related analytes, such as protein kinases and human immunodeficiency virus (HIV)

Chemosensitivity testing using microplate adenosine triphosphate-based luminescence measurements.

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During the last two decades, novel nonclonogenic methods for pretherapeutic chemosensitivity testing have been developed that are likely to overcome major technical limitations of older assays such as low evaluability rates, low degree of standardization and reproducibility, lack of technical

Phase II study of MLN8237 (Alisertib) in advanced/metastatic sarcoma.

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Aurora kinase A (AURKA) is commonly overexpressed in sarcoma. The inhibition of AURKA by shRNA or by a specific AURKA inhibitor blocks in vitro proliferation of multiple sarcoma subtypes. MLN8237 (alisertib) is a novel oral adenosine triphosphate-competitive AURKA inhibitor. This Cancer Therapy

Tumour regression after treatment with aminated beta 1-3D polyglucose is initiated by circulatory failure.

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Meth A sarcoma grew progressively when inoculated intradermally in CB6 mice. When the mice were treated on day 7 after inoculation with 10 mg aminated polyglucose (AG) [Bogwald, J., Hoffman, J. & Seljelid, R. Carbohydrate Res. 148, 101, 1986], the tumours regressed completely in over 90% of the

Increased glucose uptake capacity of Rous-transformed cells and the relevance of deprivation derepression.

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The increased rate of glucose uptake found in cells transformed by Rous sarcoma virus was shown to be enhanced relative to the changes in uptake induced in nontransformed cells by deprivation of glucose (deprivation derepression). Glucose-specific uptake sites were distinguished from

Depletion of high energy phosphate compouds in the tumor-bearing state and reversal after tumor resection.

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BACKGROUND Cancer cachexia is a syndrome manifested by a variety of metabolic abnormalities that include depletion of host energy stores. We studied liver and skeletal muscle high energy phosphate compounds, inorganic phosphorus (Pi), and the energy charge in tumor-bearing (TB), pair fed

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