acetic acid/neoplasms

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Acetic acid induces cell death: an in vitro study using normal rat gastric mucosal cell line and rat and human gastric cancer and mesothelioma cell lines.

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OBJECTIVE We recently reported that topical application of acetic acid promptly caused tumor necrosis in a mouse model of gastric cancer. The aim of the present study was to examine whether acetic acid can directly induce cancer cell death. METHODS Rat gastric epithelial cell line (RGM-1), rat

Long-term effects of flavone acetic acid on the growth of a rat tumour.

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A rat tumour (MC7 sarcoma), growing subcutaneously, has been shown to be sensitive to a single application of flavone acetic acid. Thirteen rats were still alive after 50 days and 8 of these were tumour free, as compared with control rats which survived for 15.7 +/- 2.53 days. The 8 tumour free

Flavone acetic acid (NSC 347512)-induced modulation of murine tumor physiology monitored by in vivo nuclear magnetic resonance spectroscopy.

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Flavone acetic acid (FAA), a new drug with broad activity against transplanted solid tumors of mice, induces nonrepairable DNA single strand breaks that correlate with therapeutic efficacy. To test the hypothesis that the inability of the cells to repair single strand breaks is associated with a

Acetic acid, a potent stimulator of mouse epidermal macromolecular synthesis and hyperplasia but with weak tumor-promoting ability.

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The effects of a single application of various dose levels of acetic acid or the weak tumor promoter, phorbol-12,13-ditetradecanoate, on the incorporation of tritiated thymidine (3H-TDR), 3H-cytidine, and 3H-leucine into DNA, RNA, and protein of mouse epidermis, respectively, were determined and

Rat tumor response to the vascular-disrupting agent 5,6-dimethylxanthenone-4-acetic acid as measured by dynamic contrast-enhanced magnetic resonance imaging, plasma 5-hydroxyindoleacetic acid levels, and tumor necrosis.

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The dose-dependent effects of 5,6-dimethylxanthenone-4-acetic acid (DMXAA) on rat GH3 prolactinomas were investigated in vivo. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) was used to assess tumor blood flow/permeability pretreatment and 24 hours posttreatment with 0, 100, 200, or

Tumor apoptosis by indole-3-acetic acid/light in B16F10 melanoma-implanted nude mice.

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Recently, we reported that UVB-activated indole-3-acetic acid (IAA) induces the apoptosis of G361 human melanoma cells. In the present study, we used IAA and visible light combinations to treat B16F10 melanoma-implanted nude mice using an experimental intense pulsed light (IPL) therapy model. We

5-Fluoroindole-3-acetic acid: a prodrug activated by a peroxidase with potential for use in targeted cancer therapy.

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Indole-3-acetic acid and some derivatives are oxidized by horseradish peroxidase, forming a radical-cation that rapidly fragments (eliminating CO(2)) to form cytotoxic products. No toxicity is seen when either indole-3-acetic acid or horseradish peroxidase is incubated alone at concentrations that

Assessment of the early effects of 5,6-dimethylxanthenone-4-acetic acid using macromolecular contrast media-enhanced magnetic resonance imaging: ectopic versus orthotopic tumors.

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OBJECTIVE To investigate the early effects of a vascular disrupting agent (VDA) in ectopic and orthotopic tumors by using macromolecular contrast media (MMCM)-enhanced magnetic resonance imaging (MMCM-MRI). METHODS The MMCM-MRI of ectopic and orthotopic MCA205 murine fibrosarcomas was performed

Experimental photodynamic therapy for liver cancer cell-implanted nude mice by an indole-3-acetic acid and intense pulsed light combination.

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Recently, indole-3-acetic acid (IAA) has been introduced as a new cancer therapeutic agent through oxidative decarboxylation by horseradish peroxidase (HRP). The purpose of this study was to determine the therapeutic feasibility of IAA/light combination against liver cancer. SK-HEP-1 cells were

The relationship of indole-3-acetic acid content and growth of crown-gall tumor tissues of tobacco in culture.

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We have measured the content of the auxin, indole-3-acetic acid (IAA), in cloned, crown-gall teratoma line of Nicotiana tabacum L. cv. "Turkish" by a highly specific and sensitive radioimmunoassay. This tissue line, which does not require auxin for continuous growth in culture, exhibits two phases

Structure-activity relationships for substituted 9-oxo-9,10-dihydroacridine-4-acetic acids: analogues of the colon tumour active agent xanthenone-4-acetic acid.

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A series of 9-oxo-9,10-dihydroacridine-4-acetic acids (acridone-4-acetic acids) were prepared by Jourdan-Ullmann condensation of 2-halobenzoic acids with 2-aminophenylacetic acids, followed by H2SO4-induced cyclodehydration of the resulting 2-[2-(carboxymethyl)phenylamino]benzoic acids. These were

Acetic acid, a potent agent of tumor progression in the multistage mouse skin model for chemical carcinogenesis.

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Acetic acid, a very weak tumor promoter in the multistage mouse skin model for chemical carcinogenesis, was found to be very effective at enhancing cancer development, when applied during the progression phase of the model. Papilloma-bearing mice when repeatedly treated with acetic acid had a

Therapeutic effect of transcatheter arterial chemoembolization and percutaneous injection of acetic acids on primary liver cancer.

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BACKGROUND The resection rate of primary liver tumor in China is only about 20%. A lot of patients with moderate and advanced liver tumor may lose the chance of operation. The objective of present research was to study the efficacy of transcatheter arterial chemoembolization (TACE) combined with

Percutaneous ablation of VX2 carcinoma-induced liver tumors with use of ethanol versus acetic acid: pilot study in a rabbit model.

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OBJECTIVE Acetic acid has been employed as a chemical ablation agent for liver tumors because of its superior diffusion characteristics compared with ethanol and the resulting requirement for smaller volumes and fewer injection sessions. Early tissue changes were compared after injection of acetic

Flavone acetic acid potentiates the induction of endothelial procoagulant activity by tumour necrosis factor.

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Treatment of human umbilical vein endothelial cells with flavone acetic acid (FAA) at 800 micrograms/ml for 4 h resulted in a 3-11-fold increase in procoagulant activity. This increase was due to enhanced tissue factor expression on the endothelial cell surface, as evidenced by the blocking of the

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