Next-Generation Sequencing of CYP2C19 in Stent Thrombosis: Implications for Clopidogrel Pharmacogenomics
Purpose Describe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to clopidogrel resistance. Evaluate the impact of CYP2C19 genetic variation detected by next-generation sequencing (NGS) with comprehensive annota...
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| Vydáno v: | Cardiovascular drugs and therapy Ročník 35; číslo 3; s. 549 - 559 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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New York
Springer US
01.06.2021
Springer Nature B.V |
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| ISSN: | 0920-3206, 1573-7241, 1573-7241 |
| On-line přístup: | Získat plný text |
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| Abstract | Purpose
Describe
CYP2C19
sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to clopidogrel resistance. Evaluate the impact of
CYP2C19
genetic variation detected by next-generation sequencing (NGS) with comprehensive annotation and functional studies.
Methods
Seventy ST cases on clopidogrel identified from the PLATO trial (
n
= 58) and Mayo Clinic biorepository (
n
= 12) were matched 1:1 with controls for age, race, sex, diabetes mellitus, presentation, and stent type. NGS was performed to cover the entire
CYP2C19
gene. Assessment of exonic variants involved measuring in vitro protein expression levels. Intronic variants were evaluated for potential splicing motif variations.
Results
Poor metabolizers (
n
= 4) and rare
CYP2C19*8
,
CYP2C19*15
, and
CYP2C19*11
alleles were identified only in ST cases.
CYP2C19*17
heterozygote carriers were observed more frequently in cases (
n
= 29) than controls (
n
= 18). Functional studies of
CYP2C19
exonic variants (
n
= 11) revealed 3 cases and only 1 control carrying a deleterious variant as determined by in vitro protein expression studies. Greater intronic variation unique to ST cases (
n
= 169) compared with controls (
n
= 84) was observed with predictions revealing 13 allele candidates that may lead to a potential disruption of splicing and a loss-of-function effect of
CYP2C19
in ST cases.
Conclusion
NGS detected CYP2C19 poor metabolizers and paradoxically greater number of so-called rapid metabolizers in ST cases. Rare deleterious exonic variation occurs in 4%, and potentially disruptive intronic alleles occur in 16% of ST cases. Additional studies are required to evaluate the role of these variants in platelet aggregation and clopidogrel metabolism. |
|---|---|
| AbstractList | PURPOSE: Describe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to clopidogrel resistance. Evaluate the impact of CYP2C19 genetic variation detected by next-generation sequencing (NGS) with comprehensive annotation and functional studies.
METHODS: Seventy ST cases on clopidogrel identified from the PLATO trial (n = 58) and Mayo Clinic biorepository (n = 12) were matched 1:1 with controls for age, race, sex, diabetes mellitus, presentation, and stent type. NGS was performed to cover the entire CYP2C19 gene. Assessment of exonic variants involved measuring in vitro protein expression levels. Intronic variants were evaluated for potential splicing motif variations.
RESULTS: Poor metabolizers (n = 4) and rare CYP2C19*8, CYP2C19*15, and CYP2C19*11 alleles were identified only in ST cases. CYP2C19*17 heterozygote carriers were observed more frequently in cases (n = 29) than controls (n = 18). Functional studies of CYP2C19 exonic variants (n = 11) revealed 3 cases and only 1 control carrying a deleterious variant as determined by in vitro protein expression studies. Greater intronic variation unique to ST cases (n = 169) compared with controls (n = 84) was observed with predictions revealing 13 allele candidates that may lead to a potential disruption of splicing and a loss-of-function effect of CYP2C19 in ST cases.
CONCLUSION: NGS detected CYP2C19 poor metabolizers and paradoxically greater number of so-called rapid metabolizers in ST cases. Rare deleterious exonic variation occurs in 4%, and potentially disruptive intronic alleles occur in 16% of ST cases. Additional studies are required to evaluate the role of these variants in platelet aggregation and clopidogrel metabolism. Describe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to clopidogrel resistance. Evaluate the impact of CYP2C19 genetic variation detected by next-generation sequencing (NGS) with comprehensive annotation and functional studies. Seventy ST cases on clopidogrel identified from the PLATO trial (n = 58) and Mayo Clinic biorepository (n = 12) were matched 1:1 with controls for age, race, sex, diabetes mellitus, presentation, and stent type. NGS was performed to cover the entire CYP2C19 gene. Assessment of exonic variants involved measuring in vitro protein expression levels. Intronic variants were evaluated for potential splicing motif variations. Poor metabolizers (n = 4) and rare CYP2C19*8, CYP2C19*15, and CYP2C19*11 alleles were identified only in ST cases. CYP2C19*17 heterozygote carriers were observed more frequently in cases (n = 29) than controls (n = 18). Functional studies of CYP2C19 exonic variants (n = 11) revealed 3 cases and only 1 control carrying a deleterious variant as determined by in vitro protein expression studies. Greater intronic variation unique to ST cases (n = 169) compared with controls (n = 84) was observed with predictions revealing 13 allele candidates that may lead to a potential disruption of splicing and a loss-of-function effect of CYP2C19 in ST cases. NGS detected CYP2C19 poor metabolizers and paradoxically greater number of so-called rapid metabolizers in ST cases. Rare deleterious exonic variation occurs in 4%, and potentially disruptive intronic alleles occur in 16% of ST cases. Additional studies are required to evaluate the role of these variants in platelet aggregation and clopidogrel metabolism. Purpose Describe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to clopidogrel resistance. Evaluate the impact of CYP2C19 genetic variation detected by next-generation sequencing (NGS) with comprehensive annotation and functional studies. Methods Seventy ST cases on clopidogrel identified from the PLATO trial ( n = 58) and Mayo Clinic biorepository ( n = 12) were matched 1:1 with controls for age, race, sex, diabetes mellitus, presentation, and stent type. NGS was performed to cover the entire CYP2C19 gene. Assessment of exonic variants involved measuring in vitro protein expression levels. Intronic variants were evaluated for potential splicing motif variations. Results Poor metabolizers ( n = 4) and rare CYP2C19*8 , CYP2C19*15 , and CYP2C19*11 alleles were identified only in ST cases. CYP2C19*17 heterozygote carriers were observed more frequently in cases ( n = 29) than controls ( n = 18). Functional studies of CYP2C19 exonic variants ( n = 11) revealed 3 cases and only 1 control carrying a deleterious variant as determined by in vitro protein expression studies. Greater intronic variation unique to ST cases ( n = 169) compared with controls ( n = 84) was observed with predictions revealing 13 allele candidates that may lead to a potential disruption of splicing and a loss-of-function effect of CYP2C19 in ST cases. Conclusion NGS detected CYP2C19 poor metabolizers and paradoxically greater number of so-called rapid metabolizers in ST cases. Rare deleterious exonic variation occurs in 4%, and potentially disruptive intronic alleles occur in 16% of ST cases. Additional studies are required to evaluate the role of these variants in platelet aggregation and clopidogrel metabolism. Describe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to clopidogrel resistance. Evaluate the impact of CYP2C19 genetic variation detected by next-generation sequencing (NGS) with comprehensive annotation and functional studies.PURPOSEDescribe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to clopidogrel resistance. Evaluate the impact of CYP2C19 genetic variation detected by next-generation sequencing (NGS) with comprehensive annotation and functional studies.Seventy ST cases on clopidogrel identified from the PLATO trial (n = 58) and Mayo Clinic biorepository (n = 12) were matched 1:1 with controls for age, race, sex, diabetes mellitus, presentation, and stent type. NGS was performed to cover the entire CYP2C19 gene. Assessment of exonic variants involved measuring in vitro protein expression levels. Intronic variants were evaluated for potential splicing motif variations.METHODSSeventy ST cases on clopidogrel identified from the PLATO trial (n = 58) and Mayo Clinic biorepository (n = 12) were matched 1:1 with controls for age, race, sex, diabetes mellitus, presentation, and stent type. NGS was performed to cover the entire CYP2C19 gene. Assessment of exonic variants involved measuring in vitro protein expression levels. Intronic variants were evaluated for potential splicing motif variations.Poor metabolizers (n = 4) and rare CYP2C19*8, CYP2C19*15, and CYP2C19*11 alleles were identified only in ST cases. CYP2C19*17 heterozygote carriers were observed more frequently in cases (n = 29) than controls (n = 18). Functional studies of CYP2C19 exonic variants (n = 11) revealed 3 cases and only 1 control carrying a deleterious variant as determined by in vitro protein expression studies. Greater intronic variation unique to ST cases (n = 169) compared with controls (n = 84) was observed with predictions revealing 13 allele candidates that may lead to a potential disruption of splicing and a loss-of-function effect of CYP2C19 in ST cases.RESULTSPoor metabolizers (n = 4) and rare CYP2C19*8, CYP2C19*15, and CYP2C19*11 alleles were identified only in ST cases. CYP2C19*17 heterozygote carriers were observed more frequently in cases (n = 29) than controls (n = 18). Functional studies of CYP2C19 exonic variants (n = 11) revealed 3 cases and only 1 control carrying a deleterious variant as determined by in vitro protein expression studies. Greater intronic variation unique to ST cases (n = 169) compared with controls (n = 84) was observed with predictions revealing 13 allele candidates that may lead to a potential disruption of splicing and a loss-of-function effect of CYP2C19 in ST cases.NGS detected CYP2C19 poor metabolizers and paradoxically greater number of so-called rapid metabolizers in ST cases. Rare deleterious exonic variation occurs in 4%, and potentially disruptive intronic alleles occur in 16% of ST cases. Additional studies are required to evaluate the role of these variants in platelet aggregation and clopidogrel metabolism.CONCLUSIONNGS detected CYP2C19 poor metabolizers and paradoxically greater number of so-called rapid metabolizers in ST cases. Rare deleterious exonic variation occurs in 4%, and potentially disruptive intronic alleles occur in 16% of ST cases. Additional studies are required to evaluate the role of these variants in platelet aggregation and clopidogrel metabolism. PurposeDescribe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to clopidogrel resistance. Evaluate the impact of CYP2C19 genetic variation detected by next-generation sequencing (NGS) with comprehensive annotation and functional studies.MethodsSeventy ST cases on clopidogrel identified from the PLATO trial (n = 58) and Mayo Clinic biorepository (n = 12) were matched 1:1 with controls for age, race, sex, diabetes mellitus, presentation, and stent type. NGS was performed to cover the entire CYP2C19 gene. Assessment of exonic variants involved measuring in vitro protein expression levels. Intronic variants were evaluated for potential splicing motif variations.ResultsPoor metabolizers (n = 4) and rare CYP2C19*8, CYP2C19*15, and CYP2C19*11 alleles were identified only in ST cases. CYP2C19*17 heterozygote carriers were observed more frequently in cases (n = 29) than controls (n = 18). Functional studies of CYP2C19 exonic variants (n = 11) revealed 3 cases and only 1 control carrying a deleterious variant as determined by in vitro protein expression studies. Greater intronic variation unique to ST cases (n = 169) compared with controls (n = 84) was observed with predictions revealing 13 allele candidates that may lead to a potential disruption of splicing and a loss-of-function effect of CYP2C19 in ST cases.ConclusionNGS detected CYP2C19 poor metabolizers and paradoxically greater number of so-called rapid metabolizers in ST cases. Rare deleterious exonic variation occurs in 4%, and potentially disruptive intronic alleles occur in 16% of ST cases. Additional studies are required to evaluate the role of these variants in platelet aggregation and clopidogrel metabolism. |
| Author | Zhang, Lingxin Klee, Eric W. Storey, Robert F. Jenkins, Gregory D. Wang, Liewei Weinshilboum, Richard Goel, Kashish Roger, Veronique L. Rihal, Charanjit S. Eckloff, Bruce W. Eriksson, Niclas Sicotte, Hugues Baheti, Saurabh James, Stefan Bielinski, Suzette J. Wallentin, Lars Goodman, Shaun G. Morales-Rosado, Joel A. Åkerblom, Axel Black, John L. Johnson, Stephen Pereira, Naveen L. |
| AuthorAffiliation | 1 Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA 3 Vanderbilt University School of Medicine, Nashville, TN 37215, USA 7 Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK 10 Medical Genome Facility, Mayo Clinic, Rochester, MN, USA 12 Department of Cardiovascular Medicine, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA 11 Division of Epidemiology, Mayo Clinic, Department of Health Sciences Research, Rochester, MN, USA 6 Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA 2 Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA 8 St. Michael’s Hospital, University of Toronto, Toronto, Canada 9 Canadian VIGOUR Centre, University of Alberta, Edmonton, Canada 4 Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA 5 Department of Medical Sciences, Cardiology and Uppsala Clinical Rese |
| AuthorAffiliation_xml | – name: 6 Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA – name: 11 Division of Epidemiology, Mayo Clinic, Department of Health Sciences Research, Rochester, MN, USA – name: 10 Medical Genome Facility, Mayo Clinic, Rochester, MN, USA – name: 1 Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA – name: 5 Department of Medical Sciences, Cardiology and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden – name: 9 Canadian VIGOUR Centre, University of Alberta, Edmonton, Canada – name: 4 Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA – name: 8 St. Michael’s Hospital, University of Toronto, Toronto, Canada – name: 3 Vanderbilt University School of Medicine, Nashville, TN 37215, USA – name: 12 Department of Cardiovascular Medicine, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA – name: 2 Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA – name: 7 Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK |
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| CitedBy_id | crossref_primary_10_3390_jpm11050400 crossref_primary_10_1146_annurev_pharmtox_051921_092701 crossref_primary_10_2217_pgs_2021_0058 crossref_primary_10_3389_fphar_2023_1286764 crossref_primary_10_3390_jpm11111226 crossref_primary_10_1186_s40360_024_00750_w crossref_primary_10_1016_j_bios_2022_114138 |
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| Keywords | Stent thrombosis CYP2C19 Intronic Translational medicine Pharmacogenomics |
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| PublicationTitle | Cardiovascular drugs and therapy |
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Describe
CYP2C19
sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to... Describe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to... PurposeDescribe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to... PURPOSE: Describe CYP2C19 sequencing results in the largest series of clopidogrel-treated cases with stent thrombosis (ST), the closest clinical phenotype to... |
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| SubjectTerms | Aged Alleles Annotations Cardiology Clopidogrel Clopidogrel - administration & dosage Clopidogrel - pharmacokinetics CYP2C19 Cytochrome P-450 CYP2C19 - genetics Diabetes mellitus Drug Resistance - genetics Evaluation Exome - genetics Female Genetic diversity Heterozygotes Humans Impact resistance Implants Intronic Introns Male Medicine Medicine & Public Health Middle Aged Next-generation sequencing Original Article Pharmacogenomics Phenotypes Platelet aggregation Platelet Aggregation Inhibitors - administration & dosage Platelet Aggregation Inhibitors - pharmacokinetics Protein expression Proteins Stent thrombosis Stents Thrombosis Thrombosis - prevention & control Translational medicine |
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| Title | Next-Generation Sequencing of CYP2C19 in Stent Thrombosis: Implications for Clopidogrel Pharmacogenomics |
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