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  • 1
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Deutscher Kongress für Orthopädie und Unfallchirurgie; 74. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 96. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie, 51. Tagung des Berufsverbandes der Fachärzte für Orthopädie; 20101026-20101029; Berlin; DOCPO15-1403 /20101021/
    Publication Date: 2010-10-22
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 2
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  4. Wissenschaftlicher Kongress der Deutschen Gesellschaft für Essstörungen; 20140320-20140322; Leipzig; DOC14dgess065 /20140317/
    Publication Date: 2014-03-18
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 3
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  81. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20100512-20100516; Wiesbaden; DOC10hnod482 /20100422/
    Publication Date: 2010-04-23
    Keywords: ddc: 610
    Type: conferenceObject
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  • 4
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  80. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20090520-20090524; Rostock; DOC09hnod038 /20090417/
    Publication Date: 2009-04-25
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 5
    Keywords: CANCER ; EXPRESSION ; carcinoma ; CELL ; Germany ; human ; LUNG ; lung cancer ; LUNG-CANCER ; EXPOSURE ; RISK ; GENE ; PROTEIN ; METABOLISM ; TISSUE ; PATIENT ; RISK-FACTORS ; FREQUENCY ; polymorphism ; SUSCEPTIBILITY ; PROMOTER ; OVARIAN-CANCER ; WOMEN ; MEN ; risk factors ; smoking ; PROSTATE-CANCER ; cancer risk ; RISK FACTOR ; CYP3A4 ; LINKAGE DISEQUILIBRIUM ; CANCER-PATIENTS ; CARCINOMAS ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; ADENOCARCINOMAS ; CARRIERS ; case-control studies ; CLINICAL PRESENTATION ; CYP3A,genetic polymorphism,lung cancer susceptibility,small cell lung cancer,LightCycler ; EXPRESSED HUMAN CYTOCHROME-P450S ; GENETIC VARIANT ; HUMAN LIVER-MICROSOMES ; PROSTATE TUMORS ; PROTEIN LEVELS ; squamous cell carcinoma ; TOBACCO
    Abstract: CYP3A isozymes are involved in tobacco carcinogen- and steroid-metabolism, and are expressed in human lung tissue showing interindividual variation in expression and activity. The CYP3A4* 1 B allele has been associated with a two-fold higher promoter activity and with high-grade prostate cancers. The very frequent intron 3 polymorphism in the CYP3A5 gene (CYP3A5*3) results in decreased CYP3A5 protein levels. A case-control study was conducted in 801 Caucasian lung cancer patients that included 330 adenocarcinomas, 260 squamous cell carcinomas, 171 small cell lung cancers (SCLC) and 432 Caucasian hospital-based controls. CYP3A-genotyping was performed by capillary polymerase chain reaction followed by fluorescence-based melting curve analysis. A significantly increased SCLC risk for CYP3A4* 1B allele carriers [odds ratio (OR) 2.25, 95% confidence interval (CI) 1.11-4.55, P = 0.02] was found. After dividing cases and controls by gender, an increased lung cancer risk for CYP3A4* 1B carriers (OR 3.04, 95% CI 0.94-9.90, P= 0.06) for women but not for men (OR 1.00, 95% CI 0.56-1.81) was revealed. Heavier smoking men (greater than or equal to 20 pack-years) with the CYP3A4* 1 B allele had a significant OR for lung cancer of 3.42 (95% CI 1.65-7.14, P= 0.001) compared to * 1A/1* 1A carriers with lower tobacco exposure (〈 20 pack-years). For women, the respective OR was 8.00 (95% CI 2.12-30.30, P = 0.005). Genotype frequencies were generally in Hardy-Weinberg equilibrium, except for CYP3A5 where a greater than expected number of CYP3A5* 1 homozygotes was observed among cases (P = 0.006). In addition, we observed linkage disequilibrium of CYP3A4 and CYP3A5 (P 〈 0.00001), but a nonsignificantly increased lung cancer risk was only found for homozygous CYP3A5* 1 allele carriers (OR 5.24,95% CI 0.85-102.28, P = 0.14) but not for heterozygotes. To confirm our observation that the CYP3A4* 1B allele increases SCLC risk and modifies the smoking-related lung cancer risk in a gender-specific manner, further studies, including CYP3A haplotype analysis, will be necessary. Pharmacogenetics 13:607-618 (C) 2003 Lippincott Williams Wilkins
    Type of Publication: Journal article published
    PubMed ID: 14515059
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  • 6
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; CELL ; COMBINATION ; Germany ; LUNG ; LUNG-CANCER ; RISK ; GENE ; GENES ; DRUG ; PATIENT ; MESSENGER-RNA ; IMPACT ; prognosis ; RISK-FACTORS ; CYCLE ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; FREQUENCIES ; MEMBRANE ; SNP ; chemotherapy ; LOCALIZATION ; pharmacokinetic ; PHARMACOKINETICS ; CISPLATIN ; lung neoplasms ; PHASE-II ; SINGLE ; REGRESSION ; SINGLE NUCLEOTIDE POLYMORPHISMS ; PHARMACOGENETICS ; GENOTYPE ; RISK-FACTOR ; PROGRESSION-FREE SURVIVAL ; ABCG2 ; ABCC3 ; CONCENTRATIVE NUCLEOSIDE TRANSPORTER ; PLATINUM-BASED CHEMOTHERAPY ; CELL-LUNG-CANCER ; predictive factor ; CNT1 ; multidrug resistance-associated proteins ; RESISTANCE-ASSOCIATED PROTEIN-3 ; SCLC
    Abstract: The prognosis of lung cancer patients treated with chemotherapy is poor, motivating the search for predictive factors. Single nucleotide polymorphisms (SNPs) in membrane transporter genes could influence the pharmacokinetics of cytostatic drugs and therefore affect treatment outcome. We examined 6 SNPs with known or suspected phenotypic effect: ABCG2 G34A, C421A; ABCC3 C-211T, G3890A, C3942T and CNT1 G565A. For 349 Caucasian patients with primary lung cancer [161 small cell lung cancer (SCLC), 187 nonsmall cell lung cancer (NSCLC) and 1 mixed] receiving first-line chemotherapy 3 different endpoints were analyzed: response after the 2nd cycle (R), progression-free survival (PFS) and overall survival (OS). The prognostic value of the SNPs was analyzed using multivariable logistic regression, calculating odds ratios (ORs) when comparing genotype frequencies in responders and nonresponders after the 2nd cycle. Hazard ratios (HRs) for PFS and for OS were calculated using Cox regression methods. In all lung cancer patients, none of the investigated polymorphisms modified response statistically significant. The only significant result in the histological subpopulations was in SCLC patients carrying the ABCC3 -211T allele who showed significantly worsened PFS (HR: 1.79; 95% confidence interval (CI) 1.13-2.82). In an exploratory subgroup analysis significantly worse OS was seen for carriers of the ABCG2 421A-allele treated with platinum-based drugs (HR: 1.60; 95% CI 1.04-2.47; n = 256). In conclusion, this study prioritizes ABCC3 C-211T and ABCG2 C421A as candidate transporter SNPs to be further investigated as possible predictors of the clinical outcome of chemotherapy in lung cancer patients. (C) 2008 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 19107936
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  • 7
    Keywords: DISEASE ; POPULATION ; GENETIC POLYMORPHISMS ; SUSCEPTIBILITY ; ACID ; WOMEN ; REGION ; CARCINOGENS ; DNA-ADDUCTS ; VARIANT
    Abstract: MPO participates in the metabolic activation of tobacco carcinogens such as PAHs. A frequent MPO -463 G--〉A polymorphism in the promoter region reduces MPO transcription and has been correlated with 〉4-fold lower benzo[a]pyrene-DNA adduct levels in the skin of coal tar-treated patients. Four of 7 case-control studies found significantly reduced lung cancer risk associated with the A allele. Due to their different etiologies, we examined whether the MPO genotype affects histologic lung cancer types differentially. A case-control study was conducted in 625 ever-smoking lung cancer patients, including 228 adenocarcinomas, 224 SCCs, 135 SCLCs and 340 ever-smoking hospital controls. MPO genotyping was performed by capillary PCR followed by fluorescence-based melting curve analysis. Combining the MPO -463 (G/A+A/A) genotypes, a protective effect approaching significance (OR = 0.75, 95% CI 0.55-1.01) was observed when comparing all lung cancer cases to controls. Among histologic types of lung cancer, a weak protective effect was found for both adenocarcinoma (OR = 0.81, CI 0.55-1.19) and SCC (OR = 0.82, CI 0.56-1.21); a stronger and significant effect was found for SCLC (OR = 0.58, CI 0.36-0.95; p = 0.029). Our results also suggest that the MPO genotype varies among inflammatory nonmalignant lung diseases. In conclusion, our results emphasize the need for a separate analysis of lung cancer histologic types and an adjustment for inflammatory nonmalignant lung diseases in future MPO-related studies. We confirm that the MPO -463 A variant affords a protective effect against lung cancer risk in smokers, which was strongest for SCLC patients.
    Type of Publication: Journal article published
    PubMed ID: 12432558
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  • 8
    Keywords: CELLS ; CELL ; Germany ; human ; TOOL ; CDNA ; GENE ; PROTEIN ; DOMAIN ; tumour ; hepatocytes ; FREQUENCY ; polymorphism ; POLYMORPHISMS ; VARIANTS ; TRANSPORT ; IDENTIFICATION ; RAT-LIVER ; GLUTATHIONE ; resistance ; UP-REGULATION ; MEMBRANE ; MUTATION ; HEPATOCYTE CANALICULAR ISOFORM ; DRUG-RESISTANCE ; MULTIDRUG-RESISTANCE ; ATP-dependent transport ; SUBSTRATE-SPECIFICITY ; VARIANT ; FUNCTIONAL-CHARACTERIZATION ; ANION TRANSPORT ; basolateral membrane,cholestasis,hepatocellular transporters,MRP3,polymorphism,SNP ; BINDING CASSETTE ; CHRONIC CONJUGATED HYPERBILIRUBINEMIA ; DUBIN-JOHNSON-SYNDROME
    Abstract: The human multidrug resistance protein 3 (MRP3, symbol ABCC3) is an ATP-binding cassette transporter that mediates the efflux of organic anions, including lipophilic substances conjugated with glucuronate, sulphate or glutathione, across the basolateral membrane of polarized cells (e.g. hepatocytes) into blood. Genetic variants of MRP3 may affect the transport of these substances out of cells. The aims of this study were: (i) to identify MRP3 polymorphisms; (ii) to functionally characterize one relatively frequent MRP3 polymorphism; and (iii) to establish whether MRP3 transports bilirubin glucuronosides. Exonic nucleotide variants in the ABCC3 gene were identified by single-strand conformation polymorphism analysis. The 3890G〉A mutation, resulting in MRP3-Arg(1297) His, was introduced into the ABCC3 cDNA which was stably transfected into MDCKII cells. For the functional characterization of MRP3-Arg(1297) His in comparison with MRP3, ATP-dependent transport was analysed in isolated membrane vesicles. Two non- synonymous MRP3 variants were identified with an allele frequency of 0.003 for 1643T〉A (MRP3-Leu(148)Gln) and 0.08 for 3890G〉A (MRP3-Arg(1297) His). Because of the high, frequency of the 3890G〉A mutation, and because of the close proximity of Arg(1297) to the second nucleotide-binding domain, we pursued the functional characterization of the MRP3-Arg(1297)His polymorphic variant. MRP3-Arg(1297)His was correctly localized to the basolateral membrane of polarized MDCKII cells. We identified monoglucuronosyl bilirubin, bisgiucuronosyl bilirubin and leukotriene C-4 as substrates for both MRP3 and MRP3-Arg(1297)His. Dehydroepiandrosterone-3-sulphate and 17beta-glucuronosyl oestradiol were transported with similar kinetics by MRP3 and MRP3-Arg(1297) His. This experimental setup provides a useful tool to analyse the functional consequences of polymorphic variants of MRP3. Pharmacogenetics 14: 213-223 (C) 2004 Lippincott Williams Wilkins
    Type of Publication: Journal article published
    PubMed ID: 15083066
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  • 9
    Keywords: COPY NUMBER, Copy number polymorphism, DELETION, DISEASE, DISEASES, DISTRIBUTIONS, ENZYME-ACTIVITY,
    Abstract: Objectives: Deletion polymorphisms of Glutathione-S-transferase (GST) M I and T I are considered risk factors for various diseases. However, most previous studies only distinguished "null" and "non-null" genotypes. Our aim was to develop a reliable. high-throughput GSTM1/T1 genotyping method able to determine allele copy numbers. Design and methods: We developed a multiplex real time PCR method to distinguish between heterozygous (1/0) and homozygous (1/1) GSTM1 and GSTT1 genotypes. The principle of relative quantification was applied and an expectation-maximisation (EM) algorithm was developed to assign one of 3 possible genotypes: 1/1, 1/0 or 0/0 for each of the two genes. Results: 1320 Caucasians were genotyped using the newly developed method. The observed genotype distributions did not deviate from the expected and were in Hardly-Weinberg equilibrium. GSTM1 duplication was detected in one sample. Conclusion: This new semiquantitative genotyping method is a sensitive and promising tool for large-scale molecular epidemiological and clinical studies. (C) 2008 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 19161997
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  • 10
    Keywords: CANCER ; EXPRESSION ; Germany ; human ; LUNG ; lung cancer ; LUNG-CANCER ; POPULATION ; RISK ; GENE ; GENES ; DRUG ; FAMILY ; GENETIC POLYMORPHISMS ; SEQUENCE ; polymorphism ; POLYMORPHISMS ; PROMOTER ; EFFICACY ; cancer risk ; REGION ; CARRIERS ; VARIANT ; ALLELE ; CHINESE ; CYP3AP1,CYP3A5,CYP3A4,pseudogene,polymorphism,linkage disequilibrium
    Abstract: Genetic polymorphisms of the human CYP3A family affect clinical drug efficacy and may modify cancer risk. CYP3A genes show high sequence similarity that had previously lead to misallocation of CYP3A polymorphisms. Recent studies indicated a high degree of or even complete linkage for certain CYP3A alleles. Reliable LightCycler-based genotyping methods were developed and their degree of linkage in a large Caucasian population (n = 1210) investigated. Strong linkage disequilibrium was confirmed between CYP3A4, CYP3A5, and CYP3AP1 (each at P 〈 10(-5)). Contrary to some previous results claiming complete linkage between the phenotypically relevant CYP3A5(*) 1 and a variant in a pseudogene promoter region CYP3AP1(*) 1, we found among 428 controls (15 of 66) and 782 lung cancer cases (25 of 115) approximately 22% of CYP3AP1(*) 1/(*) 3 carriers to be homozygous for CYP3A5(*) 3. We conclude that contrary to previous assumptions, the CYP3AP1 genotype is not a reliable predictor for CYP3A5 activity. (C) 2004 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15050738
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