nicotinamide/sarkoma

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The radiation response of KHT sarcomas following nicotinamide treatment and carbogen breathing.

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Preclinical investigations have demonstrated that both diffusion- and perfusion-limited hypoxic cells may exist in tumors. One approach to target such hypoxic cell subpopulations is through the combined application of nicotinamide (NIC) administration and carbogen (5% CO2:95% O2) breathing. Because

Matrix Screen Identifies Synergistic Combination of PARP Inhibitors and Nicotinamide Phosphoribosyltransferase (NAMPT) Inhibitors in Ewing Sarcoma.

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Purpose: Although many cancers are showing remarkable responses to targeted therapies, pediatric sarcomas, including Ewing sarcoma, remain recalcitrant. To broaden the therapeutic landscape, we explored the in vitro response of Ewing sarcoma cell lines against a large collection of investigational

Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) with OT-82 induces DNA damage, cell death, and suppression of tumor growth in preclinical models of Ewing sarcoma

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NAMPT mediates the rate-limiting step of the NAD salvage pathway, which maintains cellular bioenergetics and provides a necessary substrate for functions essential to rapidly proliferating cancer cells. In this study, we evaluated the efficacy and mechanisms of action of OT-82, a novel, high-potency

Inhibiting effect of nicotinamide and diphosphopyridine nucleotide on the methylcholanthrene sarcoma in rats.

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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

Purification and characterization of the feline sarcoma virus tyrosine-specific kinase pp85gag-fes.

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The transforming phosphoprotein pp85gag-fes of the Snyder-Theilen strain of feline sarcoma virus (ST-FeSV) was purified in a form which exhibits tyrosine-specific kinase activity. Cell lysates of ST-FeSV-transformed mink nonproducer cells were applied to a column of DEAE-Sephacel and eluted with a

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

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

Potentiation of the antitumor activity of cisplatin in mice by 3-aminobenzamide and nicotinamide.

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3-Aminobenzamide (3AB) and nicotinamide (NA), inhibitors of adenosine-ribose transferase (ADPRT), potentiated the antitumor activity of cisplatin (DDP) on Ehrlich ascites carcinoma in mice. The mean survival times of the mice increased from 21.2-37.0 days in DDP-treated groups to 47.0-54.6 days in

Ewing sarcoma protein promotes dissociation of poly(ADP-ribose) polymerase 1 from chromatin

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Poly(ADP-ribose) polymerase 1 (PARP1) facilitates DNA damage response (DDR). While the Ewing's sarcoma breakpoint region 1 (EWS) protein fused to FLI1 triggers sarcoma formation, the physiological function of EWS is largely unknown. Here, we investigate the physiological role of EWS in regulating

Possible mechanisms involved in tumor radiosensitization following nicotinamide administration.

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Despite continued interest in the administration of nicotinamide (NA) as a tumor-specific radiosensitizer (an effect thought to be related to increases in tumor blood flow and oxygenation), little is known about the underlying mechanism(s) of this effect. The aim of this study was to investigate

The effect of nicotinamide on microregional blood flow within tumours assessed using laser Doppler probes.

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Laser Doppler probes have been used to provide real-time spatial flow mapping of microregional erythrocyte flux within the murine Sarcoma F (SaF). The results demonstrate that fluctuations in microregional red blood cell flux are a common feature of SaF tumours, with approximately 50% of regions

The effect of combined nicotinamide and carbogen treatments in human tumour xenografts: oxygenation and tumour control studies.

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OBJECTIVE This was an investigation to study the effect of giving carbogen and nicotinamide (CON) on pO2 and the radiation response of human xenografted tumours. METHODS The human xenografts were two sarcomas (ENE2 and ES3) and a glioblastoma (HTZ17). Nicotinamide (500 mg/ kg, i.p.) was administered

Increased Nicotinamide Phosphoribosyltransferase in Rhabdomyosarcomas and Leiomyosarcomas Compared to Skeletal and Smooth Muscle Tissue.

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Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in NAD synthesis and is up-regulated in several human malignancies, including breast, colon, prostate, thyroid, gastric, and several hematopoietic malignancies. In some malignancies, such as gastric, thyroid, and

Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) activity by small molecule GMX1778 regulates reactive oxygen species (ROS)-mediated cytotoxicity in a p53- and nicotinic acid phosphoribosyltransferase1 (NAPRT1)-dependent manner.

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Cancer cells undergo mitosis more frequently than normal cells and thus have increased metabolic needs, which in turn lead to higher than normal reactive oxygen species (ROS) production. Higher ROS production increases cancer cell dependence on ROS scavenging systems to balance the increased ROS.

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