Introduction: Expert groups have created dosing guidelines to facilitate the implementation of pharmacogenetic knowledge into clinical practice and commercial pharmacogenetic tests are becoming increasingly accessible. However, the extent to which these commercial tests facilitate the implementation of dosing guidelines is not clear.
Methods: Gene-drug pairs included on 22 commercial pharmacogenetic test panels were extracted and cross-referenced with the 74 gene-drug pairs with dosing guidelines in the Pharmacogenetics Knowledgebase, with particular attention given to the 28 gene-drug pairs relevant to psychiatry.
Results: On average, 70% of the 28 gene-drug pairs most relevant to psychiatry were covered by the examined tests. Six gene-drug pairs (-venlafaxine, -paroxetine, -amitriptyline, -sertraline, -citalopram, -amitriptyline) were included by all tests. Gene-drug pairs included on less than half of the test panels included -phenytoin (14%), -carbamazepine (24%), -carbamazepine (29%), and -zuclopenthixol (43%).
Discussion: Most commercial pharmacogenetic tests we examined are well-equipped to facilitate implementation of the majority of dosing guidelines relevant to psychiatry but are limited in their ability to facilitate implementation of the full spectrum of dosing guidelines currently available.
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http://dx.doi.org/10.1055/a-0863-4692 | DOI Listing |
Expert Opin Drug Metab Toxicol
January 2025
Affiliated Yueqing Hospital, Wenzhou Medical University, Wenzhou, China.
Background: The gene polymorphisms of the CYP2C9, as well as the substrate specificity of the enzyme, result in different clearances for different substrates by CYP2C9 variants.
Research Designand Methods: The CYP2C9 wild type and 38 CYP2C9 variants, expressed in insectmicrosomes, were incubated with azilsartan. The resulting metabolite,O-desethyl azilsartan, was determined by HPLC-MS/MS.
Front Genet
September 2024
Endocrinoloy Department, Peking University First Hospital Taiyuan Hospital (Taiyuan Central Hospital), Taiyuan, China.
Background: Neutrophil extracellular traps (NETs) cause delayed wound closed up in type 2 diabetes mellitus (T2DM), but the specific regulatory mechanism of NETs-related genes (NETs-RGs) in T2DM is unclear.
Methods: We acquired GSE21321 and GSE15932 datasets from gene expression omnibus (GEO) database. First, differentially expressed genes (DEGs) between T2DM and control samples of GSE21321 dataset were sifted out by differential expression analysis.
Transl Cancer Res
July 2024
Center of Clinical Laboratory Science, The Affiliated Cancer Hospital of Nanjing Medical University & Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research, Nanjing, China.
Background: Changes in gene expression are associated with malignancy. Analysis of gene expression data could be used to reveal cancer subtypes, key molecular drivers, and prognostic characteristics and to predict cancer susceptibility, treatment response, and mortality. It has been reported that inflammation plays an important role in the occurrence and development of tumors.
View Article and Find Full Text PDFPharmacogenomics
August 2024
Laboratory of Pharmacology, Medical School, Democritus University of Thrace, Dragana Campus, Alexandroupolis, 68100, Greece.
We herein inferred the genetic diversity of CYP450 isoenzymes to predict the percentage of patients who need dose adjustment in drugs used in psychiatry. Data of 784 Greek patients receiving psychiatric care who were genotyped for CYP2D6, CYP2C19, CYP1A2, CYP3A5 and CYP2C9 isoenzymes were inferred to gene-drug pairs according to the US FDA, Clinical Pharmacogenetics Implementation Consortium and Dutch Pharmacogenetics Working Group annotations and published literature. Atypical metabolism was found for 36.
View Article and Find Full Text PDFAm J Hum Genet
July 2024
Department of Computer Science, UCLA, Los Angeles, CA, USA; Department of Human Genetics, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA; Department of Computational Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA. Electronic address:
Understanding the contribution of gene-environment interactions (GxE) to complex trait variation can provide insights into disease mechanisms, explain sources of heritability, and improve genetic risk prediction. While large biobanks with genetic and deep phenotypic data hold promise for obtaining novel insights into GxE, our understanding of GxE architecture in complex traits remains limited. We introduce a method to estimate the proportion of trait variance explained by GxE (GxE heritability) and additive genetic effects (additive heritability) across the genome and within specific genomic annotations.
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