Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The average concentration of sodium is known to be elevated in some tumors relative to normal tissues, and necrosis is suspected of being a possible cause. We have performed in vivo sodium-23 magnetic resonance imaging (MRI) of IMR-5 neuroblastoma in the athymic nude mouse on a 1.9-Tesla, small-bore animal imaging system. We compared the sodium images with histologic analysis for necrosis and with proton images, chemical measurements of water and blood content, and sodium and potassium concentrations. We found that the sodium concentrations determined by MRI were proportional to the fraction of the tumor tissue that was necrotic. Correlation coefficients varied from 0.65 to 0.78, depending upon how the data were selected. With further refinement it is possible that the sodium concentration measurements determined noninvasively by MRI may have applications as part of clinical diagnosis and staging of soft tissue tumors.
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PMID:Sodium nuclear magnetic resonance imaging of neuroblastoma in the nude mouse. 205 28

Defensins induce ion channels in model lipid bilayers and permeabilize the membranes of Escherichia coli. We investigated whether similar membrane-active events occur during defensin-mediated cytolysis of tumor cells. Although defensin-treated K562 targets did not release chromium-labeled cytoplasmic components for 5-6 h, they experienced a rapid collapse (within minutes) of the membrane potential, efflux of rubidium, and influx of trypan blue. Defensin treatment also blunted the subsequent acidification response induced by nigericin, thereby further supporting the notion of enhanced transmembrane ion flow during exposure. These initial effects on the plasma membrane were not sufficient for subsequent lysis; a second phase of injury was required which involved the continued presence of defensin. The rapid membrane permeabilization phase was inhibited by azide/2-deoxyglucose, cytochalasin B, and increased concentrations of extracellular potassium and was unaffected by actinomycin-D, cycloheximide, and varying the calcium concentration. In contrast, the second phase was unaffected by cytochalasin B, inhibited by azide/2-deoxyglucose, enhanced by actinomycin D and cycloheximide, and varied with calcium concentration. These results indicate the initial adverse effect of defensins on mammalian cells occurs at the cell membrane. It is possible that the second phase of injury is mediated intracellularly by defensin that has been internalized through this leaky membrane.
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PMID:Mechanism of mammalian cell lysis mediated by peptide defensins. Evidence for an initial alteration of the plasma membrane. 205 35

Infants with large, rapidly growing tumors of the liver who exhibit preoperative signs of tumor necrosis (elevated uric acid or K+), having received no prior chemotherapy or radiation therapy, may be at risk for acute hyperkalemia during operative manipulation of the mass. In these patients, consideration should be given to careful monitoring of serum potassium throughout operative manipulation; cardiopulmonary bypass, to protect the heart from acute hyperkalemia; or to primary biopsy of the tumor with resection planned after chemotherapy. A case of fatal refractory hyperkalemia due to tumor lysis during a trisegmentectomy for hepatoblastoma in a 7-month-old girl who presented with a large, rapidly growing tumor and hyperuricemia is described.
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PMID:Fatal refractory hyperkalemia due to tumor lysis during primary resection for hepatoblastoma. 215 76

This is a preliminary report that shows that supplemental potassium partially prevents 1,2-dimethylhydrazine (DMH) induction of tumors of the small intestine in Sprague-Dawley rats. Male rats were injected weekly with 20 mg DMH/kg body wt for 20 weeks. Potassium chloride was provided in the drinking water one week before the first DMH treatment and was continued until sacrifice 14 weeks after the last DMH treatment. There were four groups of rats and they were identified as follows: DMH, DMH + K, K, and untreated control. Based on 24-hour food and water consumption data and food and water compositions, rats provided 0.5% potassium (from KCl in the drinking water) were ingesting 287.5 +/- 9.2 mg potassium per 24 hours (K/Na = 4.18) and the unsupplemented groups were ingesting 180.3 +/- 18.4 mg potassium per 24 hours (K/Na = 2.62). At sacrifice, the incidence of DMH-induced small intestinal tumors was significantly (p less than 0.05) reduced from 46% (6/13) in the DMH group to 6% (1/17) in the DMH + K group (p less than 0.05). The potassium supplement also significantly (p less than 0.05) reduced the cumulative small intestinal tumor incidence from 40% (8/20) in the DMH group to 5% (1/20) in the DMH + K group. The incidence of colon tumors and of zymbal gland tumors appeared to be reduced by the potassium supplement; however, these were not statistically significant observations (p greater than 0.05). Based on the complete blood count and other blood parameters measured, the level of potassium supplement used induced no apparent toxic effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potassium inhibition of DMH-induced small intestinal tumors in rats. 221 2

Body composition parameters were studied in different nutritional conditions in Wistar rats with experimental cancer. Results were submitted to statistical analysis. Under a hyperlipidic diet, fat increased in control rats and decreased in animals with tumor; sodium increase and potassium decrease was verified in rats with tumor. The NA/K ratio increased in both groups and the N/K ratio increased in rats with tumor under standard diet, but decreased in rats with tumor under hyperlipidic diet. Fat decreased in the animals with tumor under an aproteic diet, but sodium increased. Potassium increased in undernourished animals of both groups. The Na/K ratio increased in rats with tumor. A comparison was made according to two different standards: "fresh body weight" and "fat-free body mass". The parameters analysed showed no significant differences in body composition.
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PMID:[Body composition in various nutritional conditions. Experimental study]. 228 62

A 58-yr-old man presented with gynecomastia and elevated serum estrogens. The diagnosis of an estrogen-secreting adrenal tumor was made based upon the finding of a 4-cm left adrenal mass, elevated levels of estradiol in peripheral and left adrenal venous blood, and increased urinary 17-ketosteroids. In addition to marked elevations in estradiol and 17-ketosteroids there was an increased baseline level of 11-deoxycorticosterone and a slightly decreased level of 18-hydroxycorticosterone, suggesting the possibility of impaired P450c11 activity. The effect of ketoconazole administration (600 mg/day) for 4 weeks was studied. Urinary free cortisol and 17-ketosteroid excretion and serum testosterone levels fell acutely (1 week). Serum estradiol levels decreased gradually over the 4-week course. Plasma aldosterone levels were essentially unaltered and 18-hydroxcorticosterone levels fell gradually, but there were marked increases in 11-deoxycorticosterone and corticosterone. Coincident with the increase in 11-deoxycorticosterone there was an increase in blood pressure and a transient fall in serum potassium. We conclude that ketoconazole administration may result in a hypermineralocorticoid state. Therefore, the usefulness of ketoconazole therapy for steroid hormone-producing neoplasms will depend upon the individual tumor's steroidogenic profile.
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PMID:Feminizing adrenocortical tumor: steroid hormone response to ketoconazole. 229 65

5-(2-Acylethynyl)-2,4-dimethoxypyrimidines (3-6) were synthesized in excellent yields from 2,4-dimethoxy-5-[2-(trimethylsilyl)ethynyl]pyrimidine (2) by treatment with acid chlorides in the presence of anhydrous aluminum chloride. Compounds 3-6 were deblocked with chlorotrimethylsilane and sodium iodide in acetonitrile to the corresponding 5-[(2-acyl-1-iodo)vinyl]uracils (7-10), which on treatment with potassium hydroxide in dioxane yielded the corresponding 5-(2-acylethynyl)uracils (11-14). The 5-(2-acylethynyl)uracils were found to be active against Ehrlich ascites carcinoma (EAC) cells in vivo, the most active compounds being 5-(2-benzoylethynyl)uracil (11) and 5-(2-p-toluoylethynyl)uracil (12). The T/C values of 281 and 300 were obtained for compounds 11 and 12, respectively, in the case of mice bearing EAC cells. The 5-(2-acylethynyl)uracils have also shown in vitro activity against CCRF-CEM and L1210/0 tumor cell lines. The lead compound 5-(2-p-toluoylethynyl)uracil effectively inhibited thymidylate synthetase.
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PMID:Synthesis and biological activities of novel 5-(2-acylethynyl)uracils. 236 78

The activity of T4 5'-monodeiodinase (5'D) in the pituitary was measured in 12 patients with pituitary adenoma (3 patients with acromegaly, 2 with prolactinoma, 1 with Cushing's disease, 1 with TSH-producing tumor, and 5 with nonfunctioning tumor) and, as a control, in a patient who died of parotid cancer. The pituitaries, obtained at operation or autopsy, were homogenized in 0.1 mol/L potassium phosphate buffer, pH 7.0, and centrifuged at 800 x g. Supernatants were incubated with [125I]T4 and 20 mmol/L dithiothreitol (DTT) at 37C for 90 min. T4 5'-D was measured by the release of 125I- with the ion exchange method. The activity of T4 5'-D in the pituitaries from patients with prolactinoma and parotid cancer was dependent on protein concentration, incubation time, incubation temperature, and T4 concentration, and was labile to prior heating at 70 C for 30 min. T4 5'-D was not inhibited by 1 mmol/L propylthiouracil, but was inhibited 95% by 0.1 mmol/L iopanoic acid. The apparent Km and maximum velocity for T4 5'-D in homogenates of prolactinoma at 20 mmol/L DTT were 11 nmol/L and 1.54 pmol/mg protein.h, respectively. This reaction followed sequential-type reaction kinetics when the DTT concentration was varied. All other homogenates of pituitary tumors, except two nonfunctioning tumors, also demonstrated T4 5'-D activity. These results indicate that 1) the human pituitary express a low Km and PTU-insensitive T4 5'-D activity which is very similar to the type II enzyme activity in the rat pituitary; and 2) various types of pituitary tumor cells contain T4 5'-D activity.
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PMID:Thyroxine 5'-deiodinase in human anterior pituitary tumors. 238 Mar 33

Cat brain tumors were produced by stereotactical xenotransplantation of rat glioma clone F98 into the internal capsule of the left hemisphere. Two to four weeks after implantation, the tissue content of water, sodium, potassium, calcium, magnesium, serum albumin, serum immunoglobulin, and hemoglobin was measured in samples taken from the tumor, from peritumoral white and gray matter, and from homotopic regions of the opposite hemisphere. Extravasated serum protein content was determined by subtracting intravascular from total tissue protein, using the hemoglobin content as a marker of blood volume. The development of brain tumors was accompanied by severe vasogenic brain edema, which was clearly confined to the ipsilateral white matter. The increase of water was paralleled by an increase of sodium, calcium, and serum proteins. Potassium and magnesium content remained constant. The calculated sodium and calcium content of edema fluid approximated that of blood serum. The content of blood proteins was about 50% lower, but the ratio of albumin/immunoglobulin was the same as in blood. It is concluded that peritumoral edema is a combination of plasma ultrafiltrate and whole plasma extravasation with different modes of formation. Implications for the pathophysiology and therapy of peritumoral edema are discussed.
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PMID:Quantitative analysis of experimental peritumoral edema in cats. 239 38

Cisplatin, an effective anti-tumor agent, has significant effects on renal function including reduced glomerular filtration rate and potassium and magnesium wasting. It has been shown recently that cisplatin increases sodium conductance across the isolated frog skin, an effect which was inhibited by amiloride. The present study investigates the influence of cisplatin on the transepithelial potential difference (PD) of distal nephron segments of the rat kidney. Measurements were made under free-flow conditions and during distal microperfusion. When cisplatin was infused intravenously in a dose of 2 mg/kg/hr, the mean free-flow PD in late distal segments (cortical collecting tubules) increased from -18.5 +/- 1.4 mV (N = 37) to -31.2 +/- 1.4 mV (N = 36) (P less than 0.001). The large negative PD seen with cisplatin was abolished with intravenous amiloride, a mean PD of +0.9 +/- 1.5 mV (N = 22) (P less than 0.001) being obtained, similar to a PD of +1.9 +/- 1.5 mV (N = 39) found in control animals infused with amiloride. Perfusion of individual late distal segments with artificial plasma ultrafiltrate yielded a mean control PD of -12.4 +/- 1.2 mV (N = 21) and a significantly higher PD of -17.5 +/- 1.5 mV (N = 24) (P less than 0.01) when cisplatin (10(-3) M) was added to the perfusate. The addition of amiloride to these perfusates reduced the mean PDs to -3.2 +/- 0.5 mV (N = 19) and -3.6 +/- 0.7 mV (N = 17), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of cisplatin on the transepithelial potential difference of rat distal tubule. 241 Jun 59


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