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

With a recently described rat model technique for direct hepatic injection of tumor cells for imaging research, there were concerns that the injection itself might produce lesions detectable with magnetic resonance (MR) imaging, thereby producing false-positive results. To examine this possibility, the authors prospectively studied 14 Sprague-Dawley rats after direct hepatic injection of cells from a rat hepatoma cell line. The rats were imaged with a variety of pulse sequences before and after intravenous injection of the contrast agent manganese dipyridoxal diphosphate at a dose of 8 mumol/kg. No intrahepatic lesions could be detected with MR imaging during the first 6 days after direct hepatic injection of the tumor cells. Therefore, the direct injection technique should be accurate for evaluating various MR imaging sequences and contrast agents for early hepatic tumor detection.
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PMID:Direct hepatic tumor injection in rats: can it be used for analysis of MR imaging contrast agent? 183 62

To determine whether abnormal metabolism of L-fucose in hepatocellular carcinoma is accompanied by alterations in the activities of fucosyltransferases, the latter were determined in plasma and liver tissue of patients with this disease and in cirrhotic and normal subjects. Activities of alpha-2/alpha-3 and alpha-6-L-fucosyltransferases were all significantly greater in plasma from patients with hepatocellular carcinoma than in plasma from cirrhotic patients or normal subjects (p less than 0.025). The activity of each enzyme was dependent, to a similar extent, on Mn2+, Mg2+ and triton X-10, irrespective of the source, and all displayed pH optimums in the range of 7.5 to 8.0. In contrast, activities of alpha-2/alpha-3 fucosyltransferases were significantly lower (p less than 0.025) in homogenates prepared from tumorous liver tissue than in that prepared from nontumorous tissue from hepatocellular carcinoma and cirrhotic patients, whereas for the alpha-6 enzyme the situation was reversed (typically, tumor tissue levels were 5 pmol/hr/mg; in nontumor tissue they were 2 pmol/hr/mg). Activities of galactosyl and mannosyltransferase in tumor tissue were greater in all cases than in nontumor cirrhotic tissue. Plasma fucosyltransferases are specifically elevated in hepatocellular carcinoma but different mechanisms appear to underlie the changes seen for alpha-2/alpha-3 and alpha-6-L-fucosyltransferases.
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PMID:Fucosyltransferases: differential plasma and tissue alterations in hepatocellular carcinoma and cirrhosis. 184 14

Manganese(II)-N,N'-dipyridoxylethylenediamine-N,N'-diacetate-5,5'-bis (phosphate) (MnDPDP) is a paramagnetic complex designed for use as a hepatobiliary agent. The T1 relaxivity of MnDPDP (2.8 [mmol/L]-1.sec-1 in aqueous solution) was similar to that of gadolinium diethylenetriaminepentaacetic acid (DTPA) (4.5 [mmol/L]-1.sec-1) and gadolinium tetraazocyclodecanetetraacetic acid (DOTA) (3.8 [mmol/L]-1.sec-1). However, in liver tissue the T1 relaxivity of MnDPDP (21.7 [mmol/L]-1.sec-1) was threefold higher than that reported for Gd-DOTA (6.7 [mmol/L]-1.sec-1). Maximum liver T1 relaxation enhancement occurred 30 minutes after injection of MnDPDP, at which time 54MnDPDP biodistribution studies indicated that 13% of total body activity was in the liver. Enhanced (MnDPDP, 50 mumol/kg) MR images showed a fivefold increase in tumor-liver contrast-to-noise ratio over baseline unenhanced images. Results of the authors' acute and subchronic toxicity studies suggest that MnDPDP will be safe at the doses necessary for clinical imaging; at 10 mumol/kg, the safety factor (LD50/effective dose) for MnDPDP is 540, significantly greater than the safety factor of Gd-DTPA (ie, 60-100).
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PMID:Preclinical evaluation of MnDPDP: new paramagnetic hepatobiliary contrast agent for MR imaging. 189 38

The existence of a single or of multiple populations of glibenclamide binding sites is a subject of controversy. In the present study, radioligand binding techniques were employed to determine whether multiple populations of [3H]glibenclamide binding sites exist in pancreatic tumor (insulinoma) cells. Additional studies were performed to further characterize the binding of [3H]glibenclamide to insulinoma and cardiac membranes. [3H]Glibenclamide bound to high (0.1 nM) and low (240 nM) affinity binding sites in insulinoma membranes. The physiological relevance of multiple populations of sites is unknown. The binding of glibenclamide to insulinoma and cardiac membranes was altered by guanine nucleotides and not adenine nucleotides. This suggests glibenclamide binding can be modulated by G-proteins. Glibenclamide binding was also modulated by divalent cations. The divalent cations, Ca2+ and Zn2+, stimulated specific glibenclamide binding to cardiac and insulinoma membranes, while Mg2+ and Mn2+ enhanced cardiac binding only. Moreover, the lowering of pH from 7.4 to 6.5 was found to enhance specific glibenclamide binding. Interestingly, the magnitude of this effect was much larger in cardiac membranes. The specific nature of the regulation of glibenclamide binding by guanine nucleotides, divalent cations and pH remains to be explored.
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PMID:Modulation of [3H]glibenclamide binding to cardiac and insulinoma membranes. 191 93

The criteria for tumor-specific MRI contrast agents are considered. The metalloporphyrins have been shown to be potential tumor-specific contrast agents due to their selective retention by cancer cells. The Mn(III) water-soluble porphyrin complexes are preferred on the basis of relaxivity and stability. Protein binding in human plasma enhances the relaxivity of Mn(III)-tetraphenylsulfonato-porphyrin (MnTTPS). In preliminary work this agent was shown to enhance MRI contrast at 0.5 T in subcutaneous human colon carcinomas grown in nude mice. Here we report further evidence of enhanced contrast in the same system, and extend this work to human breast tumors in nude mice using a 2 T animal imager. Questions of metalloporphyrin stability, toxicity and dose-contrast relationship are discussed.
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PMID:Metalloporphyrin magnetic resonance contrast agents. Feasibility of tumor-specific magnetic resonance imaging. 196 73

A series of tumor localizing porphyrins was evaluated with respect to their ability to elicit cutaneous photosensitivity and systemic immunosuppression, two of the most common side effects associated with photodynamic therapy. Using the murine ear swelling response as an indicator, it was found that all the non-metalloporphyrins caused cutaneous photosensitization. Immunosuppressive effects were noted using hematoporphyrin derivative (HPD) and meso-tetra(4-sulfonatophenyl)porphine if sensitization occurred immediately after photoirradiation, but none were evident using Photofrin II (PII) or meso-tetra(4-carboxyphenyl)porphine (TCPP). Subsequent studies indicated that PII and TCPP manifested a delayed type immunosuppression similar to that found following UVB photoirradiation. Manganese (III) meso-tetra(4-sulfonatophenyl)porphine, a prototype magnetic resonance imaging contrast agent, was also evaluated because of its reported demetallation in vivo. It was found to cause neither cutaneous photosensitivity nor immunosuppression.
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PMID:Cutaneous photosensitizing and immunosuppressive effects of a series of tumor localizing porphyrins. 202 1

This report examines a possible mechanism of mouse lung tumor prophylaxis by glucocorticoids (GC). Adrenalectomy (Ax) increased, and corticosterone replacement decreased, lung tumor multiplicity when treatment was begun before administration of the carcinogen, urethan. Ax increased the 3H-thymidine labeling index of alveolar epithelial cells. Tumor multiplicity was also enhanced when urethan was administered during the period of compensatory hyperplasia that occurred in response to lung injury induced by methylcylopentadienyl manganese tricarbonyl. Thus, carcinogen-induced tumor development was amplified by stimulation of division of the target cell population. GC regulation of alveolar epithelial cell proliferation, and hence tumor susceptibility, may be mediated by the Ca++/phospholipid-dependent protein kinase (PKC).The tumor-resistant strain, C57BL/6J, has greater adrenal corticosterone content, higher epithelial cell PKC activity, and lower alveolar epithelial cell proliferation than the tumor-susceptible strain, A/J. In vitro, GC inhibit proliferation of a lung epithelial-derived cell line and increase PKC activity in that cell line. Thus, we hypothesize that GC protect against lung tumor development by increasing PKC content in the epithelial cells from which lung tumors arise; increased intracellular PKC results in decreased epithelial proliferation, and reduces the probability of induction of tumorigenesis by urethan.
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PMID:Mechanisms of glucocorticoid involvement in mouse lung tumorigenesis. 205 36

Electrothermal atomic absorption spectrophotometry was employed to measure the concentrations of manganese, platinum, and strontium in the cerebrospinal fluid (CSF) of 47 patients with brain neoplasms (34 benign and 13 malignant), 17 leukemic patients, 10 patients with lymphoma or non-cerebral solid tumors, and 27 control patients. According to the data obtained, manganese appears to be significantly (p less than 0.015) depleted from the CSF of leukemic patients, whereas platinum is diminished in CSF of patients with brain tumors, leukemia, lymphoma, or noncerebral solid tumors; the ratios for the mean CSF concentration of platinum in these tumor patients/control patients ranged between 0.52 and 0.7. There was no significant difference in CSF concentrations of strontium among the groups examined.
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PMID:Cerebrospinal fluid content of manganese, platinum, and strontium in patients with cerebral tumors, leukemia, and other noncerebral neoplasms. 221 93

There are excellent theoretical reasons why the mineral nutrients selenium, manganese, copper and zinc, known as the antioxidant minerals, may be involved in the prevention of cancer aetiogenesis. The biochemistry is discussed of the part played by the antioxidant minerals, in the wider context of the other dietary antioxidants vitamins A, E and C, and beta carotene, in preventing tissue damage caused by activated metabolites of oxygen. The likely part played by these oxygen metabolites is described and a detailed review given of the evidence that suggests a role for antioxidant minerals, notably selenium, in preventing carcinogenesis in a range of animal models. There follows a summary of the emerging epidemiological evidence that suggests clearly that low selenium intake is a risk factor in the aetiology of human cancer.
Med Oncol Tumor Pharmacother 1990
PMID:Mineral insufficiency and cancer. 223 36

Some derivatives of nickel, cadmium, and cobalt are carcinogenic in humans and/or animals but their mechanisms of action are not known. We show that they are capable of stimulating human polymorphonuclear leukocytes (PMNs), as measured by H2O2 formation, a known tumor promoter. Most effective were the carcinogens nickel subsulfide, which caused a 550% net increase in H2O2 over that formed by resting PMNs, followed by cadmium sulfide, 400%, and nickel disulfide, 200%. Nickel sulfide and cobalt sulfide caused statistically nonsignificant increases of 45 and 20%, respectively. Noncarcinogenic barium and manganese sulfides, and sulfates of nickel, cadmium, and cobalt were inactive. The enhancement of H2O2 formation by CdS and Ni3S2 (1 mumol/2.5 x 10(5) PMNs) was comparable to that mediated by the potent tumor promoter 12-O-tetradecanoylphorbol-13-acetate, used at 0.5 and 1 nM, respectively. Concurrent treatment of 12-O-tetradecanoylphorbol-13-acetate-stimulated PMNs with Ni3S2 or NiS caused a decrease in H2O2 accumulation from that expected if the effects were additive. Including catalase in the reaction mixture proved that the oxidant formed by stimulated PMNs was H2O2, whereas adding superoxide dismutase showed that superoxide was also present in PMN samples treated with NiS but not with Ni3S2. Since nickel- and cadmium-containing particulates are deposited in the lungs and cause infiltration of PMNs, the ability to activate those cells and induce H2O2 formation may contribute to their carcinogenicity.
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PMID:Carcinogenic sulfide salts of nickel and cadmium induce H2O2 formation by human polymorphonuclear leukocytes. 225 6


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