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Gréen, Henrik
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Publications (10 of 81) Show all publications
Björn, N., Sigurgeirsson, B., Svedberg, A., Pradhananga, S., Brandén, E., Koyi, H., . . . Gréen, H. (2019). Genes and variants in hematopoiesis-related pathways are associated with gemcitabine/carboplatin-induced thrombocytopenia. The Pharmacogenomics Journal
Open this publication in new window or tab >>Genes and variants in hematopoiesis-related pathways are associated with gemcitabine/carboplatin-induced thrombocytopenia
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2019 (English)In: The Pharmacogenomics Journal, ISSN 1470-269X, E-ISSN 1473-1150Article in journal (Refereed) Epub ahead of print
Abstract [en]

Chemotherapy-induced myelosuppression, including thrombocytopenia, is a recurrent problem during cancer treatments that may require dose alterations or cessations that could affect the antitumor effect of the treatment. To identify genetic markers associated with treatment-induced thrombocytopenia, we whole-exome sequenced 215 non-small cell lung cancer patients homogeneously treated with gemcitabine/carboplatin. The decrease in platelets (defined as nadir/baseline) was used to assess treatment-induced thrombocytopenia. Association between germline genetic variants and thrombocytopenia was analyzed at single-nucleotide variant (SNV) (based on the optimal false discovery rate, the severity of predicted consequence, and effect), gene, and pathway levels. These analyses identified 130 SNVs/INDELs and 25 genes associated with thrombocytopenia (P-value < 0.002). Twenty-three SNVs were validated in an independent genome-wide association study (GWAS). The top associations include rs34491125 in JMJD1C (P-value = 9.07 × 10−5), the validated variants rs10491684 in DOCK8 (P-value = 1.95 × 10−4), rs6118 in SERPINA5 (P-value = 5.83 × 10−4), and rs5877 in SERPINC1 (P-value = 1.07 × 10−3), and the genes CAPZA2 (P-value = 4.03 × 10−4) and SERPINC1 (P-value = 1.55 × 10−3). The SNVs in the top-scoring pathway “Factors involved in megakaryocyte development and platelet production” (P-value = 3.34 × 10−4) were used to construct weighted genetic risk score (wGRS) and logistic regression models that predict thrombocytopenia. The wGRS predict which patients are at high or low toxicity risk levels, for CTCAE (odds ratio (OR) = 22.35, P-value = 1.55 × 10−8), and decrease (OR = 66.82, P-value = 5.92 × 10−9). The logistic regression models predict CTCAE grades 3–4 (receiver operator characteristics (ROC) area under the curve (AUC) = 0.79), and large decrease (ROC AUC = 0.86). We identified and validated genetic variations within hematopoiesis-related pathways that provide a solid foundation for future studies using genetic markers for predicting chemotherapy-induced thrombocytopenia and personalizing treatments.

National Category
Cancer and Oncology Medical Genetics Pharmacology and Toxicology Medicinal Chemistry
Identifiers
urn:nbn:se:liu:diva-162137 (URN)10.1038/s41397-019-0099-8 (DOI)
Available from: 2019-11-20 Created: 2019-11-20 Last updated: 2019-11-20Bibliographically approved
Björn, N., Pradhananga, S., Sigurgeirsson, B., Lundberg, J., Green, H. & Sahlén, P. (2018). Comparison of Variant Calls from Whole Genome and Whole Exome Sequencing Data Using Matched Samples. Journal of Next Generation Sequencing & Applications, 5(1), 1-8
Open this publication in new window or tab >>Comparison of Variant Calls from Whole Genome and Whole Exome Sequencing Data Using Matched Samples
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2018 (English)In: Journal of Next Generation Sequencing & Applications, ISSN 2469-9853, Vol. 5, no 1, p. 1-8Article in journal (Refereed) Published
Abstract [en]

Whole exome sequencing (WES) has been extensively used in genomic research. As sequencing costs decline it is being replaced by whole genome sequencing (WGS) in large-scale genomic studies, but more comparative information on WES and WGS datasets would be valuable. Thus, we have extensively compared variant calls obtained from WGS and WES of matched germline DNA samples from 96 lung cancer patients. WGS provided more homogeneous coverage with higher genotyping quality, and identified more variants, than WES, regardless of exome coverage depth. It also called more reference variants, reflecting its power to call rare variants, and more heterozygous variants that met applied quality criteria, indicating that WGS is less prone to allelic drop outs. However, increasing WES coverage reduced the discrepancy between the WES and WGS results. We believe that as sequencing costs further decline WGS will become the method of choice even for research confined to the exome.

Keywords
Whole genome sequencing; Whole exome sequencing; Coverage; Depth; Genotyping quality; Discordant; Concordant; Variant calls; Single-nucleotide variants
National Category
Medical Genetics
Identifiers
urn:nbn:se:liu:diva-155840 (URN)
Note

DOI not working/activated: https://doi.org/10.4172/2469-9853.1000154

Available from: 2019-03-28 Created: 2019-03-28 Last updated: 2019-11-20Bibliographically approved
Haage, P., Kronstrand, R., Josefsson, M., Calistri, S., van Schaik, R. H., Green, H. & Kugelberg, F. (2018). Enantioselective pharmacokinetics of tramadol and its three main metabolites; impact of CYP2D6, CYP2B6, and CYP3A4 genotype. Pharmacology Research & Perspectives, 6(4), Article ID e00419.
Open this publication in new window or tab >>Enantioselective pharmacokinetics of tramadol and its three main metabolites; impact of CYP2D6, CYP2B6, and CYP3A4 genotype
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2018 (English)In: Pharmacology Research & Perspectives, ISSN 2052-1707, Vol. 6, no 4, article id e00419Article in journal (Refereed) Published
Abstract [en]

Tramadol is a complex drug, being metabolized by polymorphic enzymes and administered as a racemate with the (+)- and (-)-enantiomers of the parent compound and metabolites showing different pharmacological effects. The study aimed to simultaneously determine the enantiomer concentrations of tramadol, O-desmethyltramadol, N-desmethyltramadol, and N,O-didesmethyltramadol following a single dose, and elucidate if enantioselective pharmacokinetics is associated with the time following drug intake and if interindividual differences may be genetically explained. Nineteen healthy volunteers were orally administered either 50 or 100 mg tramadol, whereupon blood samples were drawn at 17 occasions. Enantiomer concentrations in whole blood were measured by LC-MS/MS and the CYP2D6,CYP2B6 and CYP3A4 genotype were determined, using the xTAG CYP2D6 Kit, pyrosequencing and real-time PCR, respectively. A positive correlation between the (+)/(-)-enantiomer ratio and time following drug administration was shown for all four enantiomer pairs. The largest increase in enantiomer ratio was observed for N-desmethyltramadol in CYP2D6 extensive and intermediate metabolizers, rising from about two to almost seven during 24 hours following drug intake. CYP2D6 poor metabolizers showed metabolic profiles markedly different from the ones of intermediate and extensive metabolizers, with large area under the concentration curves (AUCs) of the N-desmethyltramadol enantiomers and low corresponding values of the O-desmethyltramadol and N,O-didesmethyltramadol enantiomers, especially of the (+)-enantiomers. Homozygosity of CYP2B6 *5 and *6 indicated a reduced enzyme function, although further studies are required to confirm it. In conclusion, the increase in enantiomer ratios over time might possibly be used to distinguish a recent tramadol intake from a past one. It also implies that, even though (+)-O-desmethyltramadol is regarded the enantiomer most potent in causing adverse effects, one should not investigate the (+)/(-)-enantiomer ratio of O-desmethyltramadol in relation to side effects without consideration for the time that has passed since drug intake.

Place, publisher, year, edition, pages
John Wiley & Sons, 2018
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:liu:diva-152586 (URN)10.1002/prp2.419 (DOI)000442994300006 ()29992026 (PubMedID)2-s2.0-85052511964 (Scopus ID)
Available from: 2018-11-09 Created: 2018-11-09 Last updated: 2018-12-03Bibliographically approved
Sidstedt, M., Grandell, I., Boiso, S., Sanga, M., Gréen, H., Hedman, J. & Tillmar, A. (2017). Assessing the GeneRead SNP panel for analysis of low-template and PCR-inhibitory samples. Forensic Science International: Genetics Supplement Series, 6, e267-e269
Open this publication in new window or tab >>Assessing the GeneRead SNP panel for analysis of low-template and PCR-inhibitory samples
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2017 (English)In: Forensic Science International: Genetics Supplement Series, ISSN 1875-1768, E-ISSN 1875-175X, Vol. 6, p. e267-e269Article in journal (Refereed) Published
Abstract [en]

Massive parallel sequencing (MPS) is increasingly used for human identification purposes in forensic DNA laboratories. Forensic DNA samples are by nature heterogeneous and of varying quality, both concerning DNA integrity and matrices, creating a need for assays that can handle low amounts of DNA as well as impurities. Commercial short tandem repeat (STR) analysis kits for capillary electrophoresis-based separation have evolved drastically over the past years to handle low-template samples and high amounts of various PCR inhibitors. If MPS is to be used extensively in forensic laboratories there is a need to ascertain a similar performance. We have evaluated the GeneRead Individual Identity SNP panel (Qiagen) that includes 140 SNP markers, following the GeneRead DNAseq Targeted Panels V2 handbook for library preparation, applying low levels of DNA and relevant impurities. Analysis of down to 0.1 ng DNA generated SNP profiles with at least 85% called SNPs, after increasing the number of PCR cycles in the initial PCR from 20 to 24. The SNP assay handled extracts from four different DNA extraction methods, including Chelex with blood and saliva, without detrimental effects. Further, the assay was shown to tolerate relevant amounts of inhibitor solutions from soil, cigarettes, snuff and chewing gum. In conclusion, the performance of the SNP panel was satisfactory for casework-like samples. © 2017 Elsevier B.V.

Place, publisher, year, edition, pages
Elsevier, 2017
Keywords
Forensic DNA analysis; Human identification; Massive parallel sequencing; Next generation sequencing; Single nucleotide polymorphism
National Category
Analytical Chemistry
Identifiers
urn:nbn:se:liu:diva-146972 (URN)10.1016/j.fsigss.2017.09.088 (DOI)2-s2.0-85029660404 (Scopus ID)
Available from: 2018-04-09 Created: 2018-04-09 Last updated: 2018-04-09
Vikingsson, S. & Green, H. (2016). Editorial Material: Putting Designer Drugs Back in Pandoras Box: Analytical Challenges and Metabolite Identification in CLINICAL CHEMISTRY, vol 62, issue 1, pp. Clinical Chemistry, 62(1)
Open this publication in new window or tab >>Editorial Material: Putting Designer Drugs Back in Pandoras Box: Analytical Challenges and Metabolite Identification in CLINICAL CHEMISTRY, vol 62, issue 1, pp
2016 (English)In: Clinical Chemistry, ISSN 0009-9147, E-ISSN 1530-8561, Vol. 62, no 1Article in journal, Editorial material (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
AMER ASSOC CLINICAL CHEMISTRY, 2016
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-124473 (URN)10.1373/clinchem.2015.248096 (DOI)000367703400002 ()26546634 (PubMedID)
Available from: 2016-02-02 Created: 2016-02-01 Last updated: 2017-11-30
Vikingsson, S., Gréen, H., Brinkhagen, L., Mukhtar, S. & Josefsson, M. (2016). Identification of AB-FUBINACA metabolites in authentic urine samples suitable as urinary markers of drug intake using liquid chromatography quadrupole tandem time of flight mass spectrometry.. Drug Testing and Analysis, 8(9), 950-956
Open this publication in new window or tab >>Identification of AB-FUBINACA metabolites in authentic urine samples suitable as urinary markers of drug intake using liquid chromatography quadrupole tandem time of flight mass spectrometry.
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2016 (English)In: Drug Testing and Analysis, ISSN 1942-7603, E-ISSN 1942-7611, Vol. 8, no 9, p. 950-956Article in journal (Refereed) Published
Abstract [en]

Synthetic cannabinoids are a group of psychoactive drugs presently widespread among drug users in Europe. Analytical methods to measure these compounds in urine are in demand as urine is a preferred matrix for drug testing. For most synthetic cannabinoids, the parent compounds are rarely detected in urine. Therefore urinary metabolites are needed as markers of drug intake. AB-FUBINACA was one of the top three synthetic cannabinoids most frequently found in seizures and toxicological drug screening in Sweden (2013-2014). Drug abuse is also reported from several other countries such as the USA and Japan. In this study, 28 authentic case samples were used to identify urinary markers of AB-FUBINACA intake using liquid chromatography quadrupole tandem time of flight mass spectrometry and human liver microsomes. Three metabolites suitable as markers of drug intake were identified and at least two of them were detected in all but one case. In total, 15 urinary metabolites of AB-FUBINACA were reported, including hydrolxylations on the indazole ring and the amino-oxobutane moiety, dealkylations and hydrolysis of the primary amide. No modifications on the fluorobenzyl side-chain were observed. The parent compound was detected in 54% of the case samples. Also, after three hours of incubation with human liver microsomes, 77% of the signal from the parent compound remained. Copyright © 2015 John Wiley & Sons, Ltd.

Keywords
LC-MS/MS; Spice; drugs of abuse; human liver microsomes; metabolites; new psychoactive substances; synthetic cannabinoids; urine
National Category
Medicinal Chemistry
Identifiers
urn:nbn:se:liu:diva-125343 (URN)10.1002/dta.1896 (DOI)000384805600007 ()26560240 (PubMedID)
Note

Funding agencies: National Board of Forensic Medicine; Linkoping University; Linkoping physician society; Swedish Civil Contingencies Agency

Available from: 2016-02-19 Created: 2016-02-19 Last updated: 2018-01-10
Skoglund, K., Richter, J., Olsson-Stromberg, U., Bergquist, J., Aluthgedara, W., Ubhayasekera, S. J., . . . Green, H. (2016). In Vivo Cytochrome P450 3A Isoenzyme Activity and Pharmacokinetics of Imatinib in Relation to Therapeutic Outcome in Patients With Chronic Myeloid Leukemia. Therapeutic Drug Monitoring, 38(2), 230-238
Open this publication in new window or tab >>In Vivo Cytochrome P450 3A Isoenzyme Activity and Pharmacokinetics of Imatinib in Relation to Therapeutic Outcome in Patients With Chronic Myeloid Leukemia
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2016 (English)In: Therapeutic Drug Monitoring, ISSN 0163-4356, E-ISSN 1536-3694, Vol. 38, no 2, p. 230-238Article in journal (Refereed) Published
Abstract [en]

Background: Cytochrome P450 3A (CYP3A) isoenzyme metabolic activity varies between individuals and is therefore a possible candidate of influence on the therapeutic outcome of the tyrosine kinase inhibitor imatinib in patients with chronic myeloid leukemia (CML). The aim of this study was to investigate the influence of CYP3A metabolic activity on the plasma concentration and outcome of imatinib in patients with CML. Methods: Forty-three patients with CML were phenotyped for CYP3A activity using quinine as a probe drug and evaluated for clinical response parameters. Plasma concentrations of imatinib and its main metabolite, CGP74588, were determined using liquid chromatography-mass spectrometry. Results: Patients with optimal response to imatinib after 12 months of therapy did not differ in CYP3A activity compared to nonoptimal responders (quinine metabolic ratio of 14.69 and 14.70, respectively; P = 0.966). Neither the imatinib plasma concentration nor the CGP74588/imatinib ratio was significantly associated with CYP3A activity. Conclusions: The CYP3A activity does not influence imatinib plasma concentrations or the therapeutic outcome. These results indicate that although imatinib is metabolized by CYP3A enzymes, this activity is not the rate-limiting step in imatinib metabolism and excretion. Future studies should focus on other pharmacokinetic processes so as to identify the major contributor to patient variability in imatinib plasma concentrations.

Place, publisher, year, edition, pages
LIPPINCOTT WILLIAMS & WILKINS, 2016
Keywords
pharmacokinetics; chronic myeloid leukemia; imatinib; CGP74588; CYP3A
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:liu:diva-129678 (URN)10.1097/FTD.0000000000000268 (DOI)000376938000006 ()26693810 (PubMedID)
Note

Funding Agencies|Swedish Research Council; Swedish Cancer Society; Medical Research Council of Southeast Sweden; Novartis

Available from: 2016-06-27 Created: 2016-06-23 Last updated: 2018-01-10
Vikingsson, S., Strömqvist, M., Svedberg, A., Hansson, J., Höiom, V. & Gréen, H. (2016). Novel rapid liquid chromatography tandem masspectrometry method for vemurafenib and metabolites in human plasma, including metabolite concentrations at steady-state.. BMC Biomedical chromotography, 30(8), 1234-1239
Open this publication in new window or tab >>Novel rapid liquid chromatography tandem masspectrometry method for vemurafenib and metabolites in human plasma, including metabolite concentrations at steady-state.
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2016 (English)In: BMC Biomedical chromotography, ISSN 0269-3879, E-ISSN 1099-0801, Vol. 30, no 8, p. 1234-1239Article in journal (Refereed) Published
Abstract [en]

A novel, rapid and sensitive liquid chromatography tandem-mass spectrometry method for quantification of vemurafenib in human plasma, that also for the first time allows for metabolite semi-quantification, was developed and validated to support clinical trials and therapeutic drug monitoring. Vemurafenib was analysed by precipitation with methanol followed by a 1.9 min isocratic liquid chromatography tandem masspectrometry analysis using an Acquity BEH C18 column with methanol and formic acid using isotope labelled internal standards. Analytes were detected in multi reaction monitoring mode on a Xevo TQ. Semi-quantification of vemurafenib metabolites was performed using the same analytical system and sample preparation with gradient elution. The vemurafenib method was successfully validated in the range 0.5-100 µg/mL according to international guidelines. The metabolite method was partially validated due to the lack of commercially available reference materials. For the first time concentration levels at steady-state for melanoma patients treated with vemurafenib is presented. The low abundance of vemurafenib metabolites suggests that they lack clinical significance. This article is protected by copyright. All rights reserved.

Place, publisher, year, edition, pages
John Wiley & Sons, 2016
Keywords
BRAFV600E; LC-MS/MS; melanoma; metabolites;validation
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-126098 (URN)10.1002/bmc.3672 (DOI)000379971200010 ()26683023 (PubMedID)
Note

Funding agencies: Swedish Research Council [C0592901, A0671101]; Swedish Cancer Society [130335]; County Council of Ostergotland; County Council of Stockholm-Gotland; Medical Research Council of Southeast Sweden [388611]; Swedish Medical Research Council; Radiumhemmet Rese

Available from: 2016-03-14 Created: 2016-03-14 Last updated: 2018-03-26Bibliographically approved
Green, H., Hasmats, J., Kupershmidt, I., Edsgard, D., de Petris, L., Lewensohn, R., . . . Lundeberg, J. (2016). Using Whole-Exome Sequencing to Identify Genetic Markers for Carboplatin and Gemcitabine-Induced Toxicities. Clinical Cancer Research, 22(2), 366-373
Open this publication in new window or tab >>Using Whole-Exome Sequencing to Identify Genetic Markers for Carboplatin and Gemcitabine-Induced Toxicities
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2016 (English)In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 22, no 2, p. 366-373Article in journal (Refereed) Published
Abstract [en]

Purpose: Chemotherapies are associated with significant interindividual variability in therapeutic effect and adverse drug reactions. In lung cancer, the use of gemcitabine and carboplatin induces grade 3 or 4 myelosuppression in about a quarter of the patients, while an equal fraction of patients is basically unaffected in terms of myelosuppressive side effects. We therefore set out to identify genetic markers for gemcitabine/carboplatin-induced myelosuppression. Experimental Design: We exome sequenced 32 patients that suffered extremely high neutropenia and thrombocytopenia (grade 3 or 4 after first chemotherapy cycle) or were virtually unaffected (grade 0 or 1). The genetic differences/polymorphism between the groups were compared using six different bioinformatics strategies: (i) whole-exome nonsynonymous single-nucleotide variants association analysis, (ii) deviation from Hardy-Weinberg equilibrium, (iii) analysis of genes selected by a priori biologic knowledge, (iv) analysis of genes selected from gene expression meta-analysis of toxicity datasets, (v) Ingenuity Pathway Analysis, and (vi) FunCoup network enrichment analysis. Results: A total of 53 genetic variants that differed among these groups were validated in an additional 291 patients and were correlated to the patients myelosuppression. In the validation, we identified rs1453542 in OR4D6 (P = 0.0008; OR, 5.2; 95% CI, 1.8-18) as a marker for gemcitabine/carboplatin-induced neutropenia and rs5925720 in DDX53 (P = 0.0015; OR, 0.36; 95% CI, 0.17-0.71) as a marker for thrombocytopenia. Patients homozygous for the minor allele of rs1453542 had a higher risk of neutropenia, and for rs5925720 the minor allele was associated with a lower risk for thrombocytopenia. Conclusions: We have identified two new genetic markers with the potential to predict myelosuppression induced by gemcitabine/ carboplatin chemotherapy. (C)2015 AACR.

Place, publisher, year, edition, pages
AMER ASSOC CANCER RESEARCH, 2016
National Category
Medical Genetics Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-125314 (URN)10.1158/1078-0432.CCR-15-0964 (DOI)000369076500013 ()26378035 (PubMedID)
Note

Funding Agencies|European Commission [CHEMORES LSHC-CT-2007-037665]; Swedish Cancer Society; Swedish Research Council; Fondkistan; Stiftelsen Sigurd och Elsa Goljes Minne; Marcus Borgstroms stiftelse

Available from: 2016-02-24 Created: 2016-02-19 Last updated: 2018-01-10
Svedberg, A., Green, H., Vikström, A., Lundeberg, J. & Vikingsson, S. (2015). A validated liquid chromatography tandem mass spectrometry method for quantification of erlotinib, OSI-420 and didesmethyl erlotinib and semi-quantification of erlotinib metabolites in human plasma. Journal of Pharmaceutical and Biomedical Analysis, 107, 186-195
Open this publication in new window or tab >>A validated liquid chromatography tandem mass spectrometry method for quantification of erlotinib, OSI-420 and didesmethyl erlotinib and semi-quantification of erlotinib metabolites in human plasma
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2015 (English)In: Journal of Pharmaceutical and Biomedical Analysis, ISSN 0731-7085, E-ISSN 1873-264X, Vol. 107, p. 186-195Article in journal (Refereed) Published
Abstract [en]

A liquid chromatography tandem mass spectrometry method was developed and validated for quantification of erlotinib and its metabolites in human plasma. The method is suitable for therapeutic drug monitoring and pharmacokinetic studies. The substances were extracted using protein precipitation, separated on a BEH XBridge C18 column (100 x 2.1 mm, 1.7 mu m) by gradient elution at 0.7 mL/min of acetonitrile and 5 mM ammonium acetate. The concentration was determined using a Waters Xevo triple quadrupole mass spectrometer in a multi reaction monitoring mode. The total run time was 7 min. Deuterated erlotinib and OSI-597 were used as internal standard for erlotinib and its metabolites, respectively. Erlotinib, OSI-420 and didesmethyl erlotinib were quantified in the concentration range 25-5000 ng/mL, 0.5-500 ng/mL and 0.15-10 ng/mL, respectively. Precision and accuracy was less than14% except for OSI-420 at LLOQ (17%). Extraction recovery was above 89%, 99% and 89% for erlotinib, OSI-420 and didesmethyl erlotinib, respectively. The human liver microsomes generated 14 metabolites, three of them not previously reported. Twelve metabolites were measured semi-quantitatively and validated with respect to selectivity, precision and stability. (C) 2014 Elsevier B.V. All rights reserved.

Place, publisher, year, edition, pages
Elsevier, 2015
Keywords
LC-MS/MS; Human liver microsomes; Non-small cell lung cancer; EGFR; Tyrosine kinase inhibitor
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-117227 (URN)10.1016/j.jpba.2014.12.022 (DOI)000351116900024 ()25594896 (PubMedID)
Note

Funding Agencies|Swedish Research Council [C0592901, A0671101]; Swedish Cancer Society [130335]; Medical Research Council of Southeast Sweden [388611]

Available from: 2015-04-23 Created: 2015-04-21 Last updated: 2018-05-16
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