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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult rats exposed to prenatal alcohol were evaluated for their susceptibility to either hormone- or chemical-inducing tumors. In the first study, rats exposed to prenatal alcohol displayed an increased propensity to beta-estradiol (E2)-induced adenohypophyseal prolactinoma. The susceptibility was manifest as a potentiated increase in anterior pituitary weight as well as in serum prolactin levels after 1 and 3 weeks but not 5 weeks of hormone treatment. Two weeks after withdrawing the E2-implant, the prolactinoma underwent involution and serum prolactin reversed to baseline levels. The high concentrations of serum corticosterone were also reduced but did not return to baseline levels after E2 removal. In the second study, nitrosomethylbenzylamine (NMBA) was utilized to induce esophageal cancer in adult rats. There were no significant differences in tumor incidence or size between the prenatal alcohol-exposed and the pair-fed cohorts. However, the NMBA-treated prenatal alcohol-exposed rats displayed a marked decrease in thymus: body wt ratio as well as adrenal gland hyperplasia. The results suggest that no single mechanism can account for the variable susceptibility displayed by the prenatal alcohol-exposed rats to chemical carcinogens. Some of the observed changes, however, may be attributable to the long-lasting adverse effects of prenatal alcohol exposure on the well-being of the adult host.
Alcohol
PMID:Fetal alcohol exposure and adult tumorigenesis. 147 1

The influence of sodium chloride (NaCl), miso (Japanese soybean paste) and ethanol on development of intestinal metaplasia was examined. Five-week-old male CD(SD): Crj rats were treated with two 10 Gy doses of X-rays to the gastric region at a 3-day interval (total 20 Gy). After irradiation, the rats received supplementation with NaCl (1% or 10% in diet), miso (10% in diet) or ethanol (10% in drinking water) for 12 months. The number of alkaline phosphatase-positive foci of intestinal metaplasia in rats given 1% NaCl diet (Group 3) after X-rays was significantly elevated as compared to that in rats given X-rays alone (Group 1) (P < 0.01) or X-rays with 10% NaCl (Group 2) (P < 0.01). In the pyloric gland mucosae, the total numbers of metaplastic foci in rats of Group 3 were much higher than in Group 2, or after miso diet (Group 4) or ethanol supplementation (Group 5) (P < 0.01), but no difference was found between Group 2, 4 or 5 and Group 1. Atypical hyperplasia only appeared at incidences of less than 6% in Groups 1-3 and no promoting effect on gastric tumorigenesis was evident in Group 2. The present results thus showed that the occurrence of intestinal metaplasia induced by X-irradiation can be significantly increased by administration of 1% NaCl and decreased by 10% NaCl and ethanol, but this is not associated with any influence on gastric neoplasia.
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PMID:The effects of sodium chloride, miso or ethanol on development of intestinal metaplasia after X-irradiation of the rat glandular stomach. 148 41

A gastric submucosal tumor in a 56-year-old man was presumed to be heterotopic pancreas on the basis of endoscopy and endoscopic ultrasonography. To obtain a histologic diagnosis we injected ethanol at the tumor site to create an artificial ulcer. This facilitated the removal of endoscopic biopsy specimens from the submucosal layer so that histologic examination could confirm the presence of heterotopic pancreatic tissue.
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PMID:Heterotopic pancreas diagnosed by endoscopic ultrasonography and endoscopic injection of ethanol to make a histologic diagnosis. 150 Jun 62

There are many kinds of endoscopic treatment for lung cancer. In this paper the authors describe these methods and present representative cases. The first is laser treatment. There are three methods of endoscopic laser treatment. One is vaporization using high-power lasers, for example, the Nd-YAG laser. Indications for high-power laser treatment include obstructive lesions of the trachea or large bronchi with no recognizable peripheral focus. The second is photodynamic therapy (PDT) using tumor-specific photosensitizers, and low-power lasers. PDT has potential for the treatment of early stage lung cancer. The third is "laser chemotherapy," which is a new method developed by the authors using low-power lasers, e.g., He-Ne lasers, combined with chemotherapy. It is possible that antitumor drugs could be administered in doses lower than used at present. The second method is bronchofiberscopic ethanol injection therapy for stenosis or obstruction of central airways in order to obtain airway dilatation or hemostasis. The third method is brachytherapy or endobronchial radiation for central type lung cancer. We use a bronchofiberscope to place the applicator into the target bronchial lumen. Radiation therapy is performed with 60Co high dose-rate endobronchial radiation by a remote after-loading system. The value of laser treatment has been amply demonstrated and the other methods are also yielding encouraging results in the treatment of lung cancer.
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PMID:[Endoscopic treatment of lung cancer]. 150 79

Tumor-promoting phorbol esters or calcium-mobilizing receptor ligands stimulate phosphatidylcholine breakdown and in many cells this is accompanied by phospholipase D (PLD) activation. We tested whether or not a direct relationship exists between these two phenomena. Pheochromocytoma (PC12) cells were stimulated with the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate or with the calcium-mobilizing receptor ligand bradykinin in media containing 1% ethanol. The fatty acid composition of the molecular species of phosphatidylethanol (PEt), a product of PLD activation, formed in stimulated cells was compared with the molecular species of endogenous phospholipids isolated from unstimulated PC12 cells. PEt was isolated and analyzed by fast atom bombardment-mass spectrometry (FAB-MS) in the negative ion mode. Fatty acid composition and headgroup structure of the major PEt molecular ions were confirmed by linked scan analysis. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol were isolated from unstimulated cells and converted into phosphatidic acids using PLD. Mass spectra of the respective phosphatidic acids were obtained by fast atom bombardment-mass spectrometry as described above. The molecular species of PEt formed in 12-O-tetradecanoylphorbol-13-acetate- and bradykinin-stimulated PC12 cell were identical to those of phosphatidylcholine isolated from untreated cells.
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PMID:Molecular species analysis of a product of phospholipase D activation. Phosphatidylethanol is formed from phosphatidylcholine in phorbol ester- and bradykinin-stimulated PC12 cells. 151 26

The effects of acute and chronic ethanol administration on tumor progression and metastasis were studied in rat models of leukemia and breast cancer, respectively. Acute administration of 1.5-3.5 g of ethanol/kg body weight significantly reduced survival of rats injected with CRNK-16 leukemia cells in a dose-related manner. Acute administration of 2.5-3.5 g of ethanol/kg body weight, one hour before tumor inoculation, or chronic consumption of liquid diet containing ethanol for two weeks before and three weeks after tumor inoculation, significantly increased the number of lung metastases of MADB106 mammary adenocarcinoma. The ethanol-induced increase in the number of metastases was not correlated with plasma levels of corticosterone and was not altered by the opiate antagonist naltrexone. Incubation of spleen cells in vitro in the presence of ethanol, at concentrations comparable to those measured in the blood of ethanol-treated rats, significantly suppressed natural killer (NK) cell activity against MADB106 cells in a standard chromium-release assay and decreased the binding of effector to MADB106 tumor cells. However, neither acute nor chronic ethanol administration in vivo altered splenic NK activity against this tumor in the same in vitro assay, in which the ethanol would have been washed away. These results suggest that, in the presence of ethanol, tumor progression is facilitated. The possibility that this facilitation is related to ethanol-induced impairment of the normal tumoricidal interaction between NK and tumor cells is discussed.
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PMID:Ethanol increases tumor progression in rats: possible involvement of natural killer cells. 157 4

The effect of stress on the activity and level of mRNA of spermidine/spermine N1-acetyltransferase (SAT), a polyamine degradation rate-limiting enzyme, was studied in Ehrlich ascites tumor cells. When the cells were treated with sodium arsenite or ethanol for 1 h at 37 degrees C, the activity of SAT increased time- and dose-dependently. Total RNA was isolated from cells treated with stress, and the relative abundance of the SAT mRNA was measured by Northern blot analysis. The amount was comparable to those in control cells. In stress-treated cells, the biological half-life of the enzyme was 48-55 min, but 27-30 min in control cells. When cells were treated with arsenite in the presence of cycloheximide, enzyme activity did not increase. In those cells, half-life of the enzyme was shorter than in the cells treated with arsenite alone. This suggests that stress-treatment of cells enhanced SAT activity posttranslationally and that some factor(s) which was synthesized de novo during the treatment of arsenite is involved in the stabilization of the enzyme.
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PMID:Posttranslational regulation of spermidine/spermine N1-acetyltransferase with stress. 158 59

Gap junctional intercellular communication (GJIC) is recognized as playing an important role in normal cell proliferation and development. Chemically induced alteration of GJIC has been proposed to be associated with abnormal cellular growth and/or tumor promotion. Several in vitro assays are currently used to determine the effects of chemicals on GJIC between cultured mammalian cells. One of these assays, the scrape-loading dye transfer (SL/DT) technique, is based on monitoring the transfer of the fluorescent dye Lucifer yellow from one cell into adjacent cells via functional gap junctions. The objective of our study was to evaluate and compare various approaches for quantifying results obtained with the SL/DT technique. Confluent cultures of either WB rat liver epithelial cells or LC-540 rat leydig cells were exposed to the animal tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), solvent (0.1% ethanol), or culture medium for one hour at 37 degrees C prior to analysis of GJIC. Inhibition of dye transfer was clearly evident following TPA exposure. Quantification of this dye transfer was assessed via four approaches: manually counting the number of labeled cells; measuring the distance of dye travel from the scrape line; quantifying the amount of cellular dye uptake; and determining the distribution of dye away from the scrape line. Our results suggest that while the SL/DT technique can be effectively used as a tool to determine the qualitative presence or absence of GJIC, its use in quantifying changes in GJIC following chemical exposure is limited. Since concentration-dependent responses are critical in chemical testing, application of the SL/DT method should be restricted to a screening assay for qualitatively assessing the presence or absence of GJIC.
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PMID:Limitations of the scrape-loading/dye transfer technique to quantify inhibition of gap junctional intercellular communication. 159 25

Fractionation of the EtOH extract of the bark of Asimina triloba, monitoring by brine shrimp lethality, has led to the isolation and structural elucidation of a novel highly cytotoxic Annonaceous acetogenin, trilobacin [1], in addition to six known compounds: asimicin 2], bullatacin [3], bullatacinone [4], N-p-coumaroyltyramine [5], N-trans-feruloyltyramine [6], and (+)-syringaresinol [7]. Acetogenin 1 was identified as a diastereomer of asimicin [2] by spectral and chemical methods, and both 1 and 2 showed potent and selective cytotoxicities in the NCI human tumor cell line screen.
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PMID:Additional bioactive compounds and trilobacin, a novel highly cytotoxic acetogenin, from the bark of Asimina triloba. 159 81

There is considerable evidence from epidemiological studies that even moderate dietary alcohol intake increases the risk of breast cancer in women. The aim of this study was to test the hypothesis that dietary alcohol intake increases the incidence of mammary carcinoma in a rodent model. Two matched groups of female Sprague-Dawley rats were given 7,12-dimethylbenz[a]anthracene 15 mg by gavage when 50 days old. One group of 20 animals was given dietary ethanol at a dose of 4.4 g/kg/day in their drinking water. The incidence of tumors was significantly less in the group given ethanol (P less than 0.001). In those developing tumors, there was no significant difference between the two groups in the mean number of tumors per animal, the tumor growth rate or the time to the appearance of the first tumor. This study fails to support the hypothesis established by previous epidemiological studies.
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PMID:Dietary alcohol intake does not increase the incidence of experimentally induced mammary carcinoma. 160 37


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