nicotinamide/kansè

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Effect of nicotinamide on hepatic microsomal drug metabolising system in tumour-bearing rats and mice.

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Administration of nicotinamide to Wistar rats (100 mg/kg body wt.) bearing Yoshida sarcoma (ascites) tumour as well as to Swiss and CBA mice (250 mg/kg body wt.) bearing the transplantable fibrosarcoma and the spontaneously induced mammary carcinoma, respectively, was shown to bring about a reversal

Nicotinamide exerts different acute effects on microcirculatory function and tissue oxygenation in rat tumors.

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OBJECTIVE Nicotinamide has been reported to preferentially radiosensitize tumor tissue, supposedly through a reduction in tumor hypoxia. This may occur as a result of nicotinamide-induced changes in tumor blood flow and therefore the present study was undertaken to evaluate the effect of

Promoting effect of nicotinamide on the development of renal tubular cell tumors in rats initiated with diethylnitrosamine.

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Nicotinamide administered in the drinking water of male Fischer 344 rats increased the number of renal tubular cell tumors of rats treated with an i.p. injection of diethylnitrosamine (DEN) (25-mg/kg body weight). The incidence of kidneys with tumors in rats treated with DEN alone was 5%. In rats

Glucagon secretion during the development of insulin-secreting tumors induced by streptozotocin and nicotinamide.

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Serial oral glucose tolerance tests in rats treated with streptozotocin and nicotinamide showed that blood glucose levels after glucose loading were suppressed significantly 7 months after treatment as compared to those of earlier stages. Post-glucose plasma insulin levels were significantly

Effects of nicotinamide on mouse skin tumor development and its mode of action.

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Nicotinamide (NA), a naturally occurring vitamin and a protease inhibitor, has been shown to be effective in treating some skin ailments. It inhibits cell proliferation and induces cell differentiation. This report shows the effects of NA on mouse skin tumor development and on the critical events

Superoxide dismutase and nicotinamide adenine dinucleotide phosphate: quinone oxidoreductase polymorphisms and pancreatic cancer risk.

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OBJECTIVE Pancreatic carcinoma etiology and molecular pathogenesis is weakly understood. According to the assumption that genetic variation in carcinogen metabolism further modifies the risk of exposure-related cancers, an association of functional polymorphisms in oxidative stress-modifying genes

Melanoma and nonmelanoma skin cancer chemoprevention: A role for nicotinamide?

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Ultraviolet radiation (UVR) causes DNA damage in melanocytes by producing photolesions such as cyclobutane pyrimidine dimers and 8-oxo-7-hydrodeoxyguanosine. The production of reactive oxygen species by UVR also induces inflammatory cytokines that, together with the inherent immunosuppressive

Nicotinamide N-methyltransferase in non-small cell lung cancer: promising results for targeted anti-cancer therapy.

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Lung cancer, predominantly non-small cell lung cancer (NSCLC), is currently the most common cause of malignancy-related death in the world. Despite advances in both detection and treatment, its incidence rate is still increasing. Therefore, effective strategies for early detection as well as

Small Molecule Inhibitors Simultaneously Targeting Cancer Metabolism and Epigenetics: Discovery of Novel Nicotinamide Phosphoribosyltransferase (NAMPT) and Histone Deacetylase (HDAC) Dual Inhibitors.

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Cancer metabolism and epigenetics are among the most intensely pursued research areas in anticancer drug discovery. Here we report the first small molecules that simultaneously inhibit nicotinamide phosphoribosyltransferase (NAMPT) and histone deacetylase (HDAC), two important targets of cancer

Nicotinamide as a radiosensitizer in tumours and normal tissues: the importance of drug dose and timing.

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OBJECTIVE Nicotinamide is a radiation sensitizer currently undergoing clinical testing. This was an experimental study to determine the importance of drug dose and time interval between drug administration and irradiation for radiosensitization. METHODS Nicotinamide (50-500 mg/kg) was injected

Inhibition of Nicotinamide Phosphoribosyltransferase Induces Apoptosis in Estrogen Receptor-Positive MCF-7 Breast Cancer Cells.

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OBJECTIVE Tumor cells have increased turnover of nicotinamide adenine dinucleotide (NAD+), the main coenzyme in processes including adenosine diphosphate-ribosylation, deacetylation, and calcium mobilization. NAD+ is predominantly synthesized in human cells via the salvage pathway, with the first

Vitamin B Derivative (Nicotinamide)Appears to Reduce Skin Cancer Risk.

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Nicotinamide, an amide form of vitamin B3, has shown the potential to treat a variety of dermatological conditions, including acne, rosacea, and atopic dermatitis. Recent studies have demonstrated the role of nicotinamide, in both topical and oral forms, as a chemopreventive agent against skin

The enhanced apoptosis and antiproliferative response to combined treatment with valproate and nicotinamide in MCF-7 breast cancer cells.

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Acetylation of histone is a major player in epigenetic modifications, resulting in open chromatin structures and, hence, permissive conditions for transcription-factor recruitment to the promoters, followed by initiation of transcription. Histone deacetylase inhibitors arrest cancer cell growth and

Metabolic response of prostate cancer to nicotinamide phophoribosyltransferase inhibition in a hyperpolarized MR/PET compatible bioreactor.

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BACKGROUND Metabolic shifts in disease are of great interest for the development of novel therapeutics. In cancer treatment, these therapies exploit the metabolic phenotype associated with oncogenesis and cancer progression. One recent strategy involves the depletion of the cofactors needed to

Nicotinamide sensitizes human breast cancer cells to the cytotoxic effects of radiation and cisplatin.

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Poly(ADP-ribose) polymerase (PARP) inhibitors enhance the effect of DNA alkylating agents on BRCA1‑ and BRCA2-deficient cell lines. The aim of this study was to analyze the effect of the PARP inhibitor nicotinamide (NAM) on breast cancer cells with different BRCA1 expression or function, such as

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