Schirmer, Markus Anton

[["dc.bibliographiccitation.firstpage","59"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Pharmacogenetics and Genomics"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Haberl, M."],["dc.contributor.author","Suk, A."],["dc.contributor.author","Kamdem, L. K."],["dc.contributor.author","Klein, K."],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Nurnberg, P."],["dc.contributor.author","Zanger, Ulrich M."],["dc.contributor.author","Wojnowski, Leszek"],["dc.date.accessioned","2018-11-07T10:40:54Z"],["dc.date.available","2018-11-07T10:40:54Z"],["dc.date.issued","2006"],["dc.description.abstract","Cytochrome P450 3A enzymes (CYP3A) play a major role in the metabolism of steroid hormones, drugs and other chemicals, including many carcinogens. The individually variable CYP3A expression, which remains mostly unexplained, has been suggested to affect clinical phenotypes. We investigated the CYP3A locus in five ethnic groups. The degree of linkage disequilibrium (LD) differed among ethnic groups, but the most common alleles of the conserved LD regions were remarkably similar. Non-African haplotypes are few; for example, only four haplotypes account for 80% of common European Caucasian alleles. Large LD blocks of high frequencies were suggestive of selection. Accordingly, European Caucasian and Asian cohorts each contained a block of single nucleotide polymorphism (SN Ps) with very high P excess values. The overlap between these blocks in these two groups contained only two of the investigated 26 SNPs and one of them was the CYP3A4 1B allele. The region centromeric of CYP3A4 lB exhibited high haplotype homozygosity in European Caucasians as opposed to Africa n-Americans. CYP3A4 lB showed a moderate effect on CYP3A4 mRNA and protein expression, as well as on CYP3A activity assessed as (V)max of testosterone 6 beta-hydroxylation in a liver bank. Our data are consistent with a functional relevance of CYP3A4 1B and with selection against this allele in non-African populations. The elimination of CYP3A4 1B involved different parts of the CYP3A locus in European Caucasians and Asians. Because CYP3A4 is involved in the vitamin D metabolism, rickets may have been the underlying selecting factor. Pharmacogenetics and Genomics 16:59-71. (c) 2006 Lippincott Williams & Wilkins."],["dc.identifier.isi","000234277400008"],["dc.identifier.pmid","16344723"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46413"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1744-6872"],["dc.title","Genetic signature consistent with selection against the CYP3A4 1B allele in non-African populations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","323"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","British Journal of Clinical Pharmacology"],["dc.bibliographiccitation.lastpage","335"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Vormfelde, Stefan Viktor"],["dc.contributor.author","Schirmer, Markus"],["dc.contributor.author","Hagos, Yohannes"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Engelhardt, Sabine"],["dc.contributor.author","Meineke, Ingolf"],["dc.contributor.author","Burckhardt, Gerhard"],["dc.contributor.author","Nuernberg, Peter"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.date.accessioned","2018-11-07T09:17:38Z"],["dc.date.available","2018-11-07T09:17:38Z"],["dc.date.issued","2006"],["dc.description.abstract","Aims To investigate the association between torsemide renal clearance and genetic variation in the basolaterally expressed renal organic anion transporters OAT1 and OAT3 and in the luminally situated OAT4. Methods We analysed 22 polymorphisms in the OAT coding genes SLC22A6, SLC22A8 and SLC22A11 and their haplotypes and measured torsemide renal clearance in 95 healthy men. In addition, the effect of torsemide on the OAT-mediated transport was studied in vitro. Results In stably transfected HEK293 cells torsemide (100 mu m) inhibited the uptake by human OAT1, OAT3 and OAT4 by 63.1, 58.1 and 68.0%, respectively. Torsemide renal clearance ranged from 6.5 to 43.1 ml min(-1) with a log-normal distribution and a geometric mean of 15.6 ml min(-1) (15.0-16.1 +/- SEM). No clear outlier group was observed. AA carriers of the polymorphism rs11231809 in SLC22A11 had a torsemide renal clearance of 13.3 ml min(-1) (12.7-13.9) compared with 15.1 ml min(-1) (14.5-15.8) in AT and 18.0 ml min(-1) (16.7-19.5) in TT carriers (P = 0.002). The two most frequent haplotypes at SLC22A11 showed an association with torsemide renal clearance. Homozygous carriage of these two haplotypes resulted in renal clearances of 21.2 ml min(-1) (19.0-23.7) and 11.8 ml min(-1) (10.5-13.5), respectively. No association between reanl clearance and genetic variation in SLC22A6 or SLC22A8 was observed. Conclusions Genetic variation in the gene encoding the luminally expressed OAT4 rather than in the basolaterally expressed OATs may affect the renal clearance of torsemide."],["dc.identifier.doi","10.1111/j.1365-2125.2006.02655.x"],["dc.identifier.isi","000239694000011"],["dc.identifier.pmid","16934049"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28213"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0306-5251"],["dc.title","Torsemide renal clearance and genetic variation in luminal and basolateral organic anion transporters"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","557"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Human Mutation"],["dc.bibliographiccitation.lastpage","565"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Kulle, Bettina"],["dc.contributor.author","Schirmer, M"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Suk, A."],["dc.contributor.author","Becker, C."],["dc.contributor.author","Tzvetkov, Mladen"],["dc.contributor.author","Brockmöller, Jürgen"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Wojnowski, Leszek"],["dc.date.accessioned","2017-09-07T11:54:27Z"],["dc.date.available","2017-09-07T11:54:27Z"],["dc.date.issued","2005"],["dc.description.abstract","The prospect of SNP-based genomewide association analysis has been extensively discussed, but practical experiences remain limited. We performed an association study using a recently developed array of 11,555 SNPs distributed throughout the human genome. A total of 104 DNA samples were hybridized to these chips with an average call rate of 97% (range 85.3-98.6%). The resulting genomewide scans were applied to distinguish between carriers and noncarriers of 37 test variants, used as surrogates for monogenic disease traits. The test variants were not contained in the chip and had been determined by other methods. Without adjustment for multiple testing, the procedure detected 24% of the test variants, but the positive predictive value was low (2%). Adjustment for multiple testing eliminated most false-positive associations, but the share of true positive associations decreased to 10-12%. We also simulated fine-mapping of susceptibility loci by restricting testing to the immediate neighborhood of test variants (+/- 5 Mb). This increased the proportion of correctly identified test variants to 22-27%. Simulation of a bigenic inheritance reduced the sensitivity to 1%. Similarly adverse effect had reduction of allelic penetrance. In summary, we demonstrate the feasibility and considerable specificity of SNP array based association studies to detect variants underlying monogenic, highly penetrant traits. The outcome is affected by allelic frequencies of chip SNPs, by the ratio between simulated \"cases\" and \"controls,\" and by the degree of linkage disequilibrium. A major improvement is expected from raising the density of the SNP array. (c) 2005 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/humu.20174"],["dc.identifier.gro","3143839"],["dc.identifier.isi","000229456700007"],["dc.identifier.pmid","15880731"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1397"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-liss"],["dc.relation.issn","1059-7794"],["dc.title","Application of genomewide SNP arrays for detection of simulated susceptibility loci"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","300"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Clinical Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","309"],["dc.bibliographiccitation.volume","82"],["dc.contributor.author","Vormfelde, Stefan Viktor"],["dc.contributor.author","Sehrt, Daniel"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Meineke, Ingolf"],["dc.contributor.author","Tzvetkov, Mladen Vassilev"],["dc.contributor.author","Nuernberg, P."],["dc.contributor.author","Brockmoeller, Juergen"],["dc.date.accessioned","2018-11-07T10:58:47Z"],["dc.date.available","2018-11-07T10:58:47Z"],["dc.date.issued","2007"],["dc.description.abstract","There is little data on genetic predictors of loop diuretic efficacy in humans. Therefore, we investigated the diuretic effects of single oral doses of bumetanide, frusemide, and torsemide in a crossover study in 97 healthy Caucasians in relation to genetic variation in the renal sodium transporters NKCC2 (coded by SLC12A1), NCC (SLC12A3), and ENaC (three subunits coded by SCNN1A, SCNN1B, and SCNN1G). The NCC alanine 264 allele (Gly264Ala) and the most frequent SCNN1B haplotype were associated with stronger diuresis, indicating lower reabsorbing function of these alleles. The variant alleles of the tightly coupled polymorphisms rs5723 (Leu649Leu) and rs5729 in SCNN1G were associated with weaker diuresis, indicating higher activity. Extended haplotype homozygosity implied evolutionary selection of the NCC alanine 264 allele. In conclusion, acute diuretic effects of loop diuretics were affected by genetic variation in sodium transporters that, in the nephron, are located distally from NKCC2."],["dc.identifier.doi","10.1038/sj.clpt.6100131"],["dc.identifier.isi","000249062300012"],["dc.identifier.pmid","17460608"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50547"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0009-9236"],["dc.title","Genetic variation in the renal sodium transporters NKCC2, NCC, and ENaC in relation to the effects of loop diuretic drugs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3754"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","3762"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Kulle, Bettina"],["dc.contributor.author","Schirmer, Markus"],["dc.contributor.author","Schlüter, Georg"],["dc.contributor.author","Schmidt, Albrecht"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Vonhof, Stefan"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Suk, Eun-Kyung"],["dc.contributor.author","Tzvetkov, Mladen"],["dc.contributor.author","Kruger, Anke"],["dc.contributor.author","Seifert, Silvia"],["dc.contributor.author","Kloess, Marita"],["dc.contributor.author","Hahn, Heidi"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Trümper, Lorenz"],["dc.contributor.author","Brockmöller, Jürgen"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2017-09-07T11:53:40Z"],["dc.date.available","2017-09-07T11:53:40Z"],["dc.date.issued","2005"],["dc.description.abstract","Background-A significant number of patients treated with anthracyclines develop cardiotoxicity (anthracycline-induced cardiotoxicity [ACT]), mainly presenting as arrhythmias (acute ACT) or congestive heart failure (chronic ACT). There are no data on pharmacogenomic predictors of ACT. Methods and Results-We genotyped participants of the German non-Hodgkin lymphoma study (NHL-B) who were followed up for the development of heart failure for a median of > 3 years. Single-nucleotide polymorphisms (SNPs) were selected from 82 genes with conceivable relevance to ACT. Of 1697 patients, 55 developed acute and 54 developed chronic ACT (cumulative incidence of either form, 3.2%). We detected 5 significant associations with polymorphisms of the NAD(P)H oxidase and doxorubicin efflux transporters. Chronic ACT was associated with a variant of the NAD(P)H oxidase subunit NCF4 (rs1883112, -212A -> G; symbols with right-pointing arrows, as edited? odds ratio [OR], 2.5; 95% CI, 1.3 to 5.0). Acute ACT was associated with the His72Tyr polymorphism in the p22phox subunit (rs4673; OR, 2.0; 95% CI, 1.0 to 3.9) and with the variant 7508T -> A (rs13058338; OR, 2.6; 95% CI, 1.3 to 5.1) of the RAC2 subunit of the same enzyme. In agreement with these results, mice deficient in NAD( P) H oxidase activity, unlike wild-type mice, were resistant to chronic doxorubicin treatment. In addition, acute ACT was associated with the Gly671Val variant of the doxorubicin efflux transporter multidrug resistance protein 1 (MRP1) (OR, 3.6; 95% CI, 1.6 to 8.4) and with the Val1188Glu-Cys1515Tyr (rs8187694-rs8187710) haplotype of the functionally similar MRP2 (OR, 2.3; 95% CI, 1.0 to 5.4). Polymorphisms in adrenergic receptors previously demonstrated to be predictive of heart failure were not associated with ACT. Conclusions-Genetic variants in doxorubicin transport and free radical metabolism may modulate the individual risk to develop ACT."],["dc.identifier.doi","10.1161/CIRCULATIONAHA.105.576850"],["dc.identifier.gro","3143774"],["dc.identifier.isi","000233901500014"],["dc.identifier.pmid","16330681"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1325"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0009-7322"],["dc.title","NAD(P)H oxidase and multidrug resistance protein genetic polymorphisms are associated with doxorubicin-induced cardiotoxicity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","371"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Nurnberg, P."],["dc.contributor.author","Zanger, Ulrich M."],["dc.contributor.author","Wojnowski, Leszek"],["dc.date.accessioned","2018-11-07T08:29:52Z"],["dc.date.available","2018-11-07T08:29:52Z"],["dc.date.issued","2005"],["dc.format.extent","R137"],["dc.identifier.isi","000229046800570"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16758"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","46th Spring Meeting of the Deutsche-Gesellschaft-fur-Experimentelle-und-Klinische-Pharmakologie-und Toxikologie"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","0028-1298"],["dc.title","Haplotype-phenotype analysis of the CYP3A gene locus"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Pharmacogenomics Journal"],["dc.bibliographiccitation.lastpage","211"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Vormfelde, Stefan Viktor"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Meineke, Ingolf"],["dc.contributor.author","Kirchheiner, Julia"],["dc.contributor.author","Nuernberg, P."],["dc.contributor.author","Brockmoeller, Juergen"],["dc.date.accessioned","2018-11-07T11:02:08Z"],["dc.date.available","2018-11-07T11:02:08Z"],["dc.date.issued","2007"],["dc.description.abstract","In 97 unselected volunteers and two additional homozygous carriers of CYP2C9 3, we investigated the oral clearance of torsemide in relation to 37 polymorphisms at the CYP2C gene locus. Torsemide total oral clearance was linearly associated with the number of CYP2C9 3 alleles (geometric mean: 59, 40 and 20 ml/min in carriers of no, one and two alleles) and so were the methyl- and ring-hydroxylation but not the carboxylation clearance. Haplotypes including the CYP2C9 3 allele were similarly associated with the clearances but no other variant and no haplotype not including the CYP2C9 3 variant. The extended haplotype length (EHL) of the CYP2C9 haplotypes was positively associated with higher activity of the gene product. Torsemide total oral clearance was predictable with r(2) = 82.1% using plasma concentrations at 0.5, 1, 2 and 24 h. In conclusion, torsemide's biotransformation strongly depended on the CYP2C9 3 variant but no other. Higher clearance CYP2C9 haplotypes appear to be evolutionarily selected."],["dc.identifier.doi","10.1038/sj.tpj.6500410"],["dc.identifier.isi","000246815900004"],["dc.identifier.pmid","16969365"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51306"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1470-269X"],["dc.title","Genetic variation at the CYP2C locus and its association with torsemide biotransformation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","443"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pharmacogenomics"],["dc.bibliographiccitation.lastpage","453"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schirmer, Markus"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Klein, Kathrin"],["dc.contributor.author","Kulle, Bettina"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Nuernberg, Peter"],["dc.contributor.author","Zanger, Ulrich M."],["dc.contributor.author","Wojnowski, Leszek"],["dc.date.accessioned","2018-11-07T11:02:58Z"],["dc.date.available","2018-11-07T11:02:58Z"],["dc.date.issued","2007"],["dc.description.abstract","Objective: To find genetic markers of the individual cytochrome P450 (CYP)3A expression. Methods: A large collection of liver samples phenotyped for CYP3A expression and activity was genotyped for CYP3A variants. Data were analyzed for associations between CYP3A phenotypes and genotypes, and for evidence of recent selection. Results: We report associations between the hepatic CYP3A4 protein expression level, as well as its enzymatic activity, measured as verapamil N-dealkylation, and genetic polymorphisms from two regions within the CYP3A gene cluster. One region is defined by several variants, mostly located within CYP3A7, the other by a single nucleotide polymorphism in intron 7 of CYP3A4. The effects of these single nucleotide polymorphisms are sex-dependent. For example, female carriers of T alleles of the single nucleotide polymorphism rs4646437C > T in CYP3A4 intron 7 have, respectively, 5.1-fold and 2.7-fold higher expression and activity compared with male T-carriers, but only 2.2-fold and 1.4-fold higher expression and activity compared with males of genotype CC. A regression analysis indicates that the impact of these single nucleotide polymorphisms in men goes beyond the previously reported sex effect. The rs4646437C undergoes positive selection in Caucasians, as evidenced by its relative extended haplotype homozygosity value located within the uppermost percentile of a genome-wide test set of haplotypes in the same 5% frequency bin. Conclusions: Our findings reconcile the apparent contradiction between the evidence for the influence of the individual genetic makeup on CYP3A4 expression and activity suggested by clinical studies, and the failure to identify the responsible gene variants."],["dc.identifier.doi","10.2217/14622416.8.5.443"],["dc.identifier.isi","000246464800008"],["dc.identifier.pmid","17465708"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51509"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Future Medicine Ltd"],["dc.relation.issn","1462-2416"],["dc.title","Sex-dependent genetic markers of CYP3A4 expression and activity in human liver microsomes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","807"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","808"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Schluter, G."],["dc.contributor.author","Vonhof, S."],["dc.contributor.author","Kulle, Bettina"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Suk, E. K."],["dc.contributor.author","Tzvetkov, Mladen Vassilev"],["dc.contributor.author","Kloess, Marita"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Nurnberg, P."],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T10:44:43Z"],["dc.date.available","2018-11-07T10:44:43Z"],["dc.date.issued","2004"],["dc.identifier.isi","000224783504296"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47333"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","77th Scientific Meeting of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","NAD(P)H oxidase and MRP genetic polymorphisms are associated with doxorubicin-induced cardiotoxicity"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","European Journal of Clinical Pharmacology"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Vormfelde, Stefan Viktor"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Meineke, Ingolf"],["dc.contributor.author","Nurnberg, P."],["dc.contributor.author","Brockmoeller, Juergen"],["dc.date.accessioned","2018-11-07T10:54:35Z"],["dc.date.available","2018-11-07T10:54:35Z"],["dc.date.issued","2005"],["dc.format.extent","723"],["dc.identifier.isi","000232696100134"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49598"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","7th Annual Congress of Clinical Pharmacology"],["dc.relation.eventlocation","Dresen, GERMANY"],["dc.relation.issn","0031-6970"],["dc.title","Renal torasemide clearance and polymorphisms in organic anion transporters"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]