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)

Arterial ketone body ratio (AKBR) were examined in 114 cases of hepato-biliary tract diseases. AKBR of the normal control was 1.47 +/- 0.38, while it remained less than 0.7 in liver cirrhosis, hepatocellular carcinoma (HCC), alcoholic liver diseases and malignant biliary tract obstruction. AKBR correlated well with serum albumin and cholinesterase. Thirty five cases of HCC were treated with transcatheter arterial embolization (TAE), 20 cases with gelatin sponge and 15 cases without gelatin sponge. In cases with gelatin sponge AKBR decreased significantly immediately after TAE and recovered gradually during 24 hours. Without gelatin sponge AKBR decreased slightly and remained unchanged until 24 hours later. Concerning the prognosis after TAE, AKBR recovered well in cases with good prognosis, while in poor prognosis AKBR progressively decreased to below 0.3. In experimental TAE with gelatin sponge using rabbit VX2-induced liver tumor, AKBR decreased significantly. In fatal rabbit group after TAE, AKBR decreased progressively. Plasma endotoxin was also measured in TAE with experimental rabbit, AKBR and endotoxin showed reverse correlation. From these results it was suggested that the measurement of AKBR is very useful for the evaluation of efficacy and prognosis of TAE in primary liver cancer.
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PMID:[Changes in arterial ketone body ratio after transcatheter arterial embolization for hepatocellular carcinoma-clinical and experimental studies]. 217 Jul 13

Supersensitivity to depolarization produced by succinylcholine and resistance to pancuronium were observed in paretic muscles of a patient with a right frontoparietal tumor. The abnormal sensitivity to relaxants is compared with observations reported in patients with myasthenia gravis and hemiparesis. We hypothesize that upper motoneuron dysfunction may be followed by the appearance of "new" junctional receptors, which may occasional a supersensitivity to depolarization and a poor affinity for both curare and anti-acetylcholine-receptor antibodies. A decrease in acetylcholinesterase activity of "decentralized" muscles should also be considered.
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PMID:Abnormal responses to succinylcholine and pancuronium in a patient with hemiparesis. 227 86

Single-channel recording techniques have been used to examine interactions between anticholinesterases and ion channels activated by acetylcholine. Single-channel currents activated by 200 nM acetylcholine were recorded from cell-attached patches of BC3H1 mouse tumor cells grown in culture. Channels were recorded in the absence and presence of edrophonium (1-20 microM), neostigmine (2-20 microM), or pyridostigmine (10-200 microM). All three drugs shortened channel open time but did not alter single-channel current amplitude. Effects on channel open time were not secondary to inhibition of cholinesterase but appeared to involve direct interactions between anticholinesterase drugs and acetylcholine-activated channels. Drug concentrations calculated to reduce the time constant of open time distributions by 50% were 3.8 microM edrophonium, 4.6 microM neostigmine, or 97 microM pyridostigmine. Channel open time was decreased by edrophonium at concentrations comparable to those occurring during reversal of neuromuscular block, but it was reduced by neostigmine and pyridostigmine only at levels higher than those encountered clinically. Differences in interactions between anticholinesterases and acetylcholine-activated channels at the end plate may possibly account for some of the clinical differences between these drugs.
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PMID:Comparison of anticholinesterases and their effects on acetylcholine-activated ion channels. 231 31

To study the molecular origin of the altered regulation of butyrylcholinesterase (BuChE) in nervous system tumors, BuChE complementary DNA (cDNA) sequences from human glioblastoma and neuroblastoma cDNA libraries were compared with BuChE cDNAs from normal fetal and adult tissues. A single 2.6-kilobase BuChE cDNA sequence was found in all normal tissues, whereas an additional alternatively terminated BuChE cDNA clone was found in both tumor libraries. The tumor-specific cDNA contained a 3',0.7-kilobase nontranslatable extension, as well as several nucleotide alterations in the normal polyadenylation site. Single-base mutations in the coding region of this unusual BuChE cDNA infer two amino acid substitutions: Asp70----Gly and Ser425----Pro. The Asp70----Gly change has recently been implicated with "atypical" BuChE, which is deficient in its capacity to hydrolyze succinylcholine. The 3.6-kilobase mRNA was less abundant in RNA blot hybridization than the 2.6-kilobase mRNA, which is in agreement with the low ratios between the 3.6- and 2.6-kilobase BuChE cDNA clones in glioblastoma and neuroblastoma libraries. Furthermore, size fractionation and microinjection of glioblastoma polyadenylated RNA, followed by enzyme activity and selective inhibition measurements, demonstrated two peaks of functional BuChE mRNA, the heavier one probably reflecting the longer transcripts. Chromosomal mapping of the 0.7-kilobase 3' fragment by in situ hybridization localized it to a unique 3q26-ter position, where we recently found an inheritably amplified "silent" defective CHE gene in a family exposed to the cholinesterase inhibitor methyl parathion. Our findings confirm previous genetic linkage mapping of the functional CHE gene to the 3q26-ter position and demonstrate that extended functional mRNA transcripts encoding a BuChE form with two modified amino acids are produced from this gene in glioblastoma and neuroblastoma cells.
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PMID:Expression of alternatively terminated unusual human butyrylcholinesterase messenger RNA transcripts, mapping to chromosome 3q26-ter, in nervous system tumors. 231 87

A case of Takatsuki disease, 57-year-old male associated with monoclonal IgA, lambda-type immunoglobulin was treated with recombinant alpha-interferon daily by intramuscular injection with an initial dose of 3 X 10(6) U/day. Four weeks later, gynecomastia was improved and breast pain disappeared. Increases of cholesterol from 84 mg/dl to 135 mg/dl and cholinesterase from 0.24 delta pH to 0.48 delta pH were observed, 8 weeks later. Though, there was no reduction in serum M protein, no decrease in the number of bone marrow tumor cell and no restoration of muscle atrophy and polyneuropathy. No predominant side effect was observed. We conclude that rIFN alpha has a some potential role in the treatment of Takatsuki disease and additional chemotherapy should be considered. Significance of the therapy against Takatsuki disease was discussed.
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PMID:[Therapeutic effect of recombinant interferon alpha on Takatsuki disease]. 235 63

The genes for acetylcholinesterase (ACHE) and butyrylcholinesterase (CHE) are expressed in multiple tumor tissues, including ovarian carcinomas. Both CHE and ACHE genes coamplify in leukemias. To examine the relationship of gene amplification to the expression of these genes in tumors, ACHE and CHE genes and their expression were studied in primary ovarian carcinomas. DNA blot hybridization demonstrated a significant amplification and mutagenesis of both genes in 6 of 11 malignant tumors studied. This was greater or of the same order of magnitude as the amplification of the oncogenes c-rafi, v-sis, and c-fes in these tumors. No amplification was found in normal ovarian tissues or benign ovarian cysts. Xenopus oocyte microinjections, blot and in situ hybridizations, and immuno- and cytochemical staining revealed translatable CHEmRNA and its active protein product in discrete tumor foci. The frequent coamplification in ovarian carcinomas of ACHE and CHE genes implicates cholinesterases in neoplastic growth and/or proliferation.
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PMID:Acetylcholinesterase and butyrylcholinesterase genes coamplify in primary ovarian carcinomas. 239 39

Cholinesterases are ubiquitous carboxylesterase type B enzymes capable of hydrolyzing the neurotransmitter acetylcholine which are transiently expressed in multiple germline, embryonic, and tumor cells. The acute poisoning effects of various organophosphorous compounds are generally attributed to their irreversible covalent interaction with cholinesterases and block of their catalytic activities. We have recently found a de novo inheritable amplification of a CHE gene encoding defective butyrylcholinesterase (acylcholine acyl hydrolase; EC 3.1.1.8) in a family under prolonged exposure to the agricultural organophosphorous insecticide methyl parathion. Further analysis revealed that both the CHE and the ACHE genes, encoding acetylcholinesterase (acetylcholine acetyl hydrolase; EC 3.1.1.7), are amplified in leukemias and platelet disorders and that the tumorigenic expression of these genes in ovarian carcinomas is associated with their frequent coamplification in these tumors. The amplification of CHE and ACHE genes in normal and tumor tissues might be analogous to the well-known amplification of other genes encoding target proteins to toxic compounds. As such, it could provide cells a selection advantage when exposed to organophosphorous poisons. Further, since cholinesterases appear to play developmentally important roles in multiple cell types, the amplification and overexpression of their corresponding genes might affect fertility, be related to the progression of various tumor types, and bear upon the ecological and clinical risks involved with the common use of organophosphorous poisons.
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PMID:Amplification of butyrylcholinesterase and acetylcholinesterase genes in normal and tumor tissues: putative relationship to organophosphorous poisoning. 240 80

Decay-accelerating factor (DAF) is a 70,000 Mr membrane protein that inhibits amplification of the complement cascade on the cell surface, and protects cells from damage. Purified DAF can be reincorporated into the membrane of red cells and is functional. DAF is deficient in paroxysmal nocturnal hemoglobinuria (PNH), a disease characterized by increased sensitivity of erythrocytes to complement lysis. We show here that DAF is part of a newly described family of membrane proteins anchored to the lipid bilayer by means of phosphatidylinositol (PI). Treatment with PI-specific phospholipase C (PIPLC) releases 70-80, 60, and 10% of cell surface DAF from mononuclear cells, neutrophils, and erythrocytes, respectively. The PIPLC-released DAF (DAF-S) is slightly smaller (67,000 Mr) than the membrane form. DAF and DAF-S cannot be distinguished antigenically. Furthermore, DAF-S has lost its ability to significantly inhibit the C3-convertase, as well as its ability to incorporate into cell membranes. Since DAF can only inhibit C3-convertase endogenously, i.e., within the membrane of the same cell, it is likely that the loss of activity of DAF-S is causally related to its inability to reincorporate in the lipid bilayer. As shown by others, the complement-sensitive red cells from PNH patients lack acetylcholinesterase, which is also anchored to the membrane by PI (9). Thus it is possible that the molecular defect in PNH lies in the biosynthetic pathways leading to the attachment of PI to the polypeptide chains, in the transport of these proteins to the surface, or in their release by the action of endogenous phospholipases. From a practical standpoint the specific release of DAF by PIPLC could facilitate killing of tumor cells by amplifying the effects of the complement cascade on the surface of antibody-sensitized cells.
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PMID:Release of decay-accelerating factor (DAF) from the cell membrane by phosphatidylinositol-specific phospholipase C (PIPLC). Selective modification of a complement regulatory protein. 242 13

The histogenesis of alveolar soft part sarcoma (ASPS) has been investigated since its description. Twenty ASPS cases were analyzed for immunohistochemical content, with emphasis directed toward the paraganglial, Schwann cell, and muscle theories of histogenesis. In addition, the cases were examined for possible prognostic clinical features. The clinical characteristics of the patients were similar to those reported previously concerning average age (23 years); male:female ratio (1:1); and predominant primary site (lower extremity, nine cases). Despite a local recurrence rate of 20% and a metastatic rate of 68% (including four at presentation), the natural history was often indolent and relapse commonly occurred very late. The average follow-up period was 10.1 years. While the overall 5-year survival was 67%, only seven of 18 patients were alive without disease at last follow-up (1.7-32 years), and one patient died of tumor after a 28-year disease-free interval. Neither tumor size nor site appeared to affect prognosis. The tumors were analyzed immunohistochemically for neurofilament, S-100 protein, met-enkephalin, leu-enkephalin, acetylcholinesterase, alpha 1-antichymotrypsin, Factor VIII-related antigen, serotonin, lysozyme, neuron-specific enolase, myoglobin, cytokeratins, desmin, and vimentin. Except for weak vimentin immunoreactivity, no other antigenic expression was detected despite multiple repeated experiments with several antibodies. S-100 protein which is present in virtually all granular cell tumors was absent in the cases of ASPS. The lack of detectable expression of neurofilament, met-enkephalin and leu-enkephalin, and neuron-specific enolase is interpreted as evidence against the paraganglial theory of histogenesis. Similarly, the repeated absence of the muscle proteins, desmin and myoglobin, in contrast to a previous report, is interpreted as evidence against a myogenic origin.
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PMID:Alveolar soft part sarcoma. A clinicopathologic and immunohistochemical study. 243 29

The paper critically analyzes available data on the nutritional and metabolic effects of total parenteral nutrition (TPN) and enteral nutrition (EN) in cachectic cancer patients. Only papers dealing with adult cancer patients and providing data regarding type of tumor, duration of the nutritional support, and administration rate of calories and amino acids, validated by statistical analysis of the results, are included. The main conclusions are the following: (1) No nutritional variable worsened in cancer patients receiving TPN or EN, in conditions in which progressive deterioration of the nutritional status is the rule. (2) The nutritional variables improved by TPN and EN were body weight, fat mass, and some indicators of lean body mass (nitrogen balance and whole body potassium). Thyroxin-binding prealbumin and retinol-binding protein increased only with TPN, whereas some immunologic indexes (complement factors and lymphocytes) improved only with EN. (3) The daily regimens which improved lean body mass and visceral proteins ranged from 35 to 55 kcal/kg and from 1.2 to 2.0 g of amino acids/kg for TPN; for EN it was 35 kcal/kg and 1.3 g of amino acids/kg. However, the enteral regimen capable of improving some immune responses included at least 42 kcal/kg and 2.3 g of amino acids/kg. (4) Only three randomized studies were performed to compare TPN and EN, and conflicting results were obtained. Only TPN showed some significant advantages with regard to weight gain, nitrogen balance, maintenance of serum albumin levels and some mineral balances. However, the advantage of TPN was not clear enough to recommend its indiscriminate use. The choice between TPN and EN should always consider the functionality of the GI tract, the need for hospitalization to start a TPN regimen, and the higher cost of intravenous feeding. (5) When comparing TPN to a standard oral diet, the following variables improved with the nutritional support: body weight, nitrogen balance, 3-methylhistidine, urinary excretion, and serum levels of transferrin, cholinesterase, thyroxin-binding prealbumin, and retinol-binding protein. (6) When comparing TPN with glucose vs TPN with glucose-lipids, no major difference was found with regard to most nutritional variables. In conclusion, nutritional support alone probably has a small role in managing a limited number of advanced cancer patients dying primarily because of malnutrition or mainly suffering from nutritional deterioration. It can also have a "permissive" role in those patients potentially candidate to an oncologic treatment which cannot be delivered because of a poor nutritional status.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of artificial nutrition on the nutritional status of cancer patients. 250 78


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