About: Study on mechanism of antineoplastic action of an anticancer drug ellipticine

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An Entity of Type : http://linked.opendata.cz/ontology/domain/vavai/Projekt, within Data Space : linked.opendata.cz associated with source document(s)

Attributes	Values
rdf:type	http://linked.opendata.cz/ontology/domain/vavai/Projekt
rdfs:seeAlso	http://www.isvav.cz/projectDetail.do?rowId=GA203/06/0329
Description	Mechanism of anticancer agent ellipticine action has not yet been precisely explained. It was suggested that the prevalent mechanisms of ellipticine are intercalation into DNA and inhibition of topoisomerase II. Recently, we found that it also covalentlybinds to DNA after being enzymatically activated. Several questions exist, which remain to be answered; whether adducts generated by ellipticine in healthy tissues are formed also in DNA of target tumor tissues and whether the adduct formation correlate with pharmacological effects. Another question is whether DNA adducts of healthy tissues might cause the genotoxic transformation in patients during their treatment. The target genes modified by ellipticine and the persistence of their modification should be identified. From the point of view of the reaction mechanism of the DNA adduct formation, it is necessary to solve the structure of the metabolites of ellipticine responsible for their formation and to characterize their structures. The project (en) Mechanismus působení kancerostatika ellipticinu není ještě zcela objasněn. Vedle působení jako interkalátor a inhibitor topoisomerasy II, může působit jako pro-léčivo, které je metabolizováno na sloučeniny kovalentně modifikující DNA. Otázkou zůstává, zda k modifikaci dochází také v cílových nádorových tkáních, a zda tato modifikace koreluje s regresí jejich vývoje. Dalším problémem je, zda DNA adukty jsou v léčbě pouze positivní skutečností či mohou-li iniciovat vedlejší genotoxické účinky. Nutné je poznat geny modifikované ellipticinem a určit, zda DNA adukty zdravých tkání jsou perzistentní, či jsou-li reparačními enzymy opravovány. Pro teoretické poznání je pak nutné identifikovat mechanismus aktivace ellipticinu a identifikovat strukturu aduktů s DNA. Poznání jejich struktury a metabolitů ellipticinu zodpovědných za jejich tvorbu je nutné pro konstrukci efektivnějšího léčiva, účinného i v nádorech, ve kterých nejsou exprimovány enzymy jeho metabolické aktivace. Odpovědět na výše uvedené otázky
Title	Study on mechanism of antineoplastic action of an anticancer drug ellipticine (en) Studium mechanismu protinádorového účinku ellipticinu
skos:notation	GA203/06/0329
http://linked.open...avai/cep/aktivita	Standard projects
http://linked.open...kovaStatniPodpora	http://linked.opendata.cz/resource/domain/vavai/projekt/GA203%2F06%2F0329/celkovaStatniPodpora
http://linked.open...ep/celkoveNaklady	http://linked.opendata.cz/resource/domain/vavai/projekt/GA203%2F06%2F0329/celkoveNaklady
http://linked.open...datumDodatniDoRIV	2009-10-22 (xsd:date)
http://linked.open...i/cep/druhSouteze	VS - Veřejná soutěž ve výzkumu a vývoji
http://linked.open...ep/duvernostUdaju	S - Úplné a pravdivé údaje nepodléhající ochraně podle zvláštních právních předpisů
http://linked.open.../cep/fazeProjektu	68674310
http://linked.open...ai/cep/hlavniObor	CE - Biochemie
http://linked.open...hodnoceniProjektu	V - Vynikající výsledky (s mezinárodním významem apod.). Zároveň byly splněny cíle a předpokládané výsledky uvedené ve smlouvě / rozhodnutí o poskytnutí podpory.
http://linked.open...vai/cep/kategorie	ZV - Základní výzkum
http://linked.open.../cep/klicovaSlova	anticancer drugs; mechanism of action; ellipticine; metabolic activation (en)
http://linked.open...ep/partnetrHlavni	Přírodovědecká fakulta
http://linked.open...inujicichPrijemcu	0 (xsd:int)
http://linked.open...cep/pocetPrijemcu	1 (xsd:int)
http://linked.open...ocetSpoluPrijemcu	0 (xsd:int)
http://linked.open.../pocetVysledkuRIV	34 (xsd:int)
http://linked.open...enychVysledkuVRIV	34 (xsd:int)
http://linked.open...lneniVMinulemRoce	2008-04-25 (xsd:date)
http://linked.open.../prideleniPodpory	http://linked.opendata.cz/resource/domain/vavai/cep/prideleniPodpory/203%2F06%2F0329
http://linked.open...iciPoslednihoRoku	2008
http://linked.open...atUdajeProjZameru	2009
http://linked.open.../vavai/cep/soutez	SGA02006GA-ST
http://linked.open...usZobrazovaneFaze	DUU
http://linked.open...ai/cep/typPojektu	P - Projekt výzkumu a vývoje financovaný ze státního rozpočtu
http://linked.open...ep/ukonceniReseni	2008-12-31 (xsd:date)
http://linked.open...ep/zahajeniReseni	2006-01-01 (xsd:date)
http://linked.open...jektu+dodavatelem	Projekt významně přispěl k poznání mechanismu působení protinádorového léčiva ellipticinu. Majoritní účinek tohoto léčiva tkví v jeho potenciálu kovalentně modifikovat DNA nádorových buněk. Takový účinek je determinován jeho metabolickou aktivací cytochr (cs) The project contributed to an increase our knowledge on mechanisms of molecular effects of anticancer drug ellipticine. The major mechanism found in the project is the covalent modfication of DNA by ellipticine in target cancer cells. Ellipticine metabol (en)
http://linked.open...tniCyklusProjektu	ZBKU
http://linked.open.../cep/klicoveSlovo	anticancer drugs ellipticine mechanism of action
is http://linked.open...vavai/riv/projekt of	Isolation of cytoplasmic NADPH-dependent phenol hydroxylase and catechol-1,2-dioxygenase from Candida tropicalis yeast Redox cycling in the metabolism of the environmental pollutant and suspected human carcinogen o-anisidine by rat and rabbit hepatic microsomes A one-electron oxidation of carcinogenic nonaminoazo dye Sudan I by horseradish peroxidase 3-Aminobenzanthrone, a human metabolite of the carcinogenic environmental pollutant 3-nitrobenzanthrone, induces biotransformation enzymes in rat kidney and lung The mechanism of cytotoxicity and DNA adduct formation by the anticancer drug ellipticine in human neuroblastoma cells The anticancer drug ellipticine is a potent inducer of rat cytochromes P450 1A1 and 1A2, thereby modulating its own metabolism The anticancer drug ellipticine is an inducer of rat NAD(P)H : Quinone oxidoreductase Comparison of the cytotoxicity of and DNA adduct formation by the anticancer drug ellipticine in human breast adenocarcinoma, leukemia and neuroblastoma cells Formation and persistence of DNA adducts of anticancer drug ellipticine in rats Effect of benzo[a]pyrene treatment on hepatic cytochrrome P450 and NADPH: cytochrrome P450 reductase (POR) levels in mice with liver-specific deletion of the POR gene Cytochromes P450 reconstituted with NADPH:P450 reductase mimic the activating and detoxicating metabolism of the anticancer drug ellipticine in microsomes The effect of pH on peroxidase-mediated oxidation of and DNA adduct formation by ellipticine Oxidation pattern of the anticancer drug ellipticine by hepatic microsomes - Similarity between human and rat systems Molecular mechanisms of antineoplastic action of an anticancer drug ellipticine DNA adducts in genotoxicology DNA adduct formation by the anticancer drug ellipticine in human leukemia HL-60 and CCRF-CEM cells Mammalian peroxidases activate anticancer drug ellipticine to intermediates forming deoxyguanosine adducts in DNA identical to those found in vivo and generated from 12-hydroxyellipticine and 13-hydroxyellipticine Role of hepatic cytochromes P450 in bioactivation of the anticancer drug ellipticine: Studies with the hepatic NADPH: Cytochrome P450 reductase null mouse Metabolic activation of benzo[a]pyrene in vitro by hepatic cytochrome P450 contrasts with detoxification in vivo: experiments with hepatic cytochrome P450 reductase null mice Structural analysis of binding of a diamantoid substrate to cytochrome P450 2B4: Possible role of Arg 133 in modulation of function and activity of this enzyme Isolation and partial characterization of the adduct formed by 13-hydroxyellipticine with deoxyguanosine in DNA Human cytochromes P450 1A1 and 1A2 participate in detoxication of carcinogenic aristolochic acid The mechanism of the different genotoxicity of the urban air pollutants 3-nitrobenzanthrone and 2-nitrobenzanthrone Rat cytochromes P450 oxidize 3-aminobenzanthrone, a human metabolite of the carcinogenic environmental pollutant 3-nitrobenzanthrone Experimental approaches to evaluate activities of cytochromes P450 3A Oxidation of carcinogenic 2-nitroanisole by rat cytochromes P450 – similarity between human and rat enzymes The comparison of cytotoxicity of the anticancer drugs doxorubicin and ellipticine to human neuroblastoma cells Optimization of preparation of apo-cytochrome b5 utilizing apo-myoglobin Cytochrome P450-mediated metabolism of N-(2-methoxyphenyl)-hydroxylamine, a human metabolite of the environmental pollutants and carcinogens o-anisidine and o-nitroanisole Contribution of Biotransformation Enzymes to the Development of Renal Injury and Urothelial Cancer Caused by Aristolochic Acid: Urgent Questions, Difficult Answers An efficient modification of ellipticine synthesis and preparation of 13-hydroxyellipticine Studies with the hepatic NADPH:cytochrome P450 reductase null mouse reveal the role of hepatic cytochromes P450 in bioactivation of the anticancer drug ellipticine Oxidation of ellipticine by human and rat cytochromes P450 correlates with its binding to DNA Metabolic activation of carcinogenic aristolochic acid, a risk factor for urothelial cancer
is http://linked.open...vavai/cep/projekt of	http://linked.opendata.cz/resource/domain/vavai/cep/ucast/GA203%2F06%2F0329/2006/orjk%3A11310 http://linked.opendata.cz/resource/domain/vavai/cep/ucast/GA203%2F06%2F0329/2007/orjk%3A11310 http://linked.opendata.cz/resource/domain/vavai/cep/ucast/GA203%2F06%2F0329/2008/orjk%3A11310 http://linked.opendata.cz/resource/domain/vavai/cep/ucast/GA203%2F06%2F0329/2009/orjk%3A11310

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