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glucose 6 phosphatase/krūties vėžys

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StraipsniaiKlinikiniai tyrimaiPatentai
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Tumor 18F-FDG incorporation is enhanced by attenuation of P53 function in breast cancer cells in vitro.

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Mutations in the p53 gene, often resulting in loss of wild-type (WT) p53 expression, are found at high frequencies in several cancer types. High uptake of (18)F-FDG detected using (18)F-FDG PET has been associated with a poor prognosis. To determine whether high (18)F-FDG uptake may be related to

Therapeutic effect of tamoxifen and energy-modulating vitamins on carbohydrate-metabolizing enzymes in breast cancer.

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BACKGROUND Cancer cells have an abnormal energetic metabolism. One of the earliest discovered hallmarks of cancer had its roots in bioenergetics, as many tumours were found in the 1920s to exhibit a high glycolytic phenotype. An animal with cancer shows significant and progressive energy loss from

Glucose-6-phosphatase Expression-Mediated [18F]FDG Efflux in Murine Inflammation and Cancer Models.

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PURPOSE
2-Deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) accumulation in inflammatory lesions can confound the diagnosis of cancer. In this study, we investigated [18F]FDG accumulation and efflux in relation to the genes and proteins involved in glucose

Influence of tamoxifen on gluconeogenesis and glycolysis in the perfused rat liver.

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The actions of tamoxifen, a selective estrogen receptor modulator used in chemotherapy and chemo-prevention of breast cancer, on glycolysis and gluconeogenesis were investigated in the isolated perfused rat liver. Tamoxifen inhibited gluconeogenesis from both lactate and fructose at very low
The aim of this study was to document the effect of hesperidin on the key enzyme activities of carbohydrate metabolism, lipid profile, and membrane-bound adenosine triphosphatases (ATPases) during 7,12-dimethylbenz(a)anthracene (DMBA)-induced breast carcinogenesis. Hesperidin has been reported to
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