Show simple item record Semsei, Ágnes F Erdélyi, Dániel Ungvári, Ildikó Csagoly E Hegyi, Márta Kiszel PS Lautner-Csorba, Orsolya Szabolcs, Judit Masat P Fekete, György Falus, András Szalai, Csaba Kovács, Gábor 2016-10-12T07:22:35Z 2016-10-12T07:22:35Z 2012
dc.identifier 84862565294
dc.identifier.citation pagination=79-86; journalVolume=36; journalIssueNumber=1; journalTitle=CELL BIOLOGY INTERNATIONAL;
dc.identifier.uri doi:10.1042/CBI20110264
dc.description.abstract Anthracyclines are potent cytostatic drugs the correct dosage of which is critical to aviod possible cardiac side effects. ABCC1 (MRP1) is expressed in the heart and takes part in the detoxification and protection of the cells from toxic effects of xenobiotics, including anthracyclines. Our objective was to search for associations between left ventricular function and single nucleotide polymorphisms of the ABCC1 gene in children who received anthracycline chemotherapy. We analyzed data of 235 pediatric patients with acute lymphoblastic leukemia. Patients were followed up by echocardiography (median follow up 6.3 years). Nine polymorphisms in the ABCC1 gene were genotyped. The ABCC1 rs3743527TT genotype and rs3743527TT-rs246221TC/TT genotype combination were found to be associated with lower left ventricular fractional shortening (LVFS) after chemotherapy. Our results suggest that genetic variants in the ABCC1 gene could influence anthracycline induced left ventricular dysfunction.
dc.relation.ispartof urn:issn:1065-6995
dc.title ABCC1 polymorphisms in anthracycline-induced cardiotoxicity in childhood acute lymphoblastic leukaemia
dc.type Journal Article 2016-10-06T12:28:33Z
dc.language.rfc3066 en
dc.identifier.mtmt 1769902
dc.identifier.wos 000299364400010
dc.identifier.pubmed 21929509
dc.contributor.department MTA TKI/MTA-SE Gyulladásbiológiai és Immungenomikai Kutatócsoport (2006-ig: MTA-SE Molekuláris Immunológiai Kutatócsoport)
dc.contributor.department SE/AOK/K/II. Sz. Gyermekgyógyászati Klinika
dc.contributor.department SE/AOK/I/Genetikai, Sejt- és Immunbiológiai Intézet
dc.contributor.institution MTA Támogatott Kutatócsoportok
dc.contributor.institution Semmelweis Egyetem

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