Aug 2026· Frontiers in Genetics· Vol 17· 0 citations· 63 references
Medicine
TL;DR
It is proposed that the strategic integration of genome-wide analyses, sequencing, multi-omics data, and hypothesis-driven genetic studies may accelerate the clinical adoption of pharmacogenetics and contribute to more effective precision medicine in psychiatry.
Abstract
The clinical adoption of pharmacogenetics has advanced unevenly despite rapid progress in genomic discovery. Genome-wide association studies and next-generation sequencing have substantially improved our understanding of the polygenic and regulatory architecture of complex diseases, yet translating these insights into clinically actionable pharmacogenetic strategies remains challenging. In this opinion article, we argue that targeted genetic approaches, traditionally represented by candidate gene association studies, should be reconsidered within a modern genomic framework. While such approaches proved limited as discovery tools for complex disease risk, they may retain translational value when integrated with genome-wide evidence and multi-omics prioritization. In pharmacogenetics, pathway-focused investigations and targeted validation studies can help bridge the gap between large-scale genomic discovery and clinical implementation. Within this framework, pharmacokinetic pharmacogenes (e.g., CYP2D6, CYP2C19) and pharmacodynamic phenotypes (e.g., treatment response, antipsychotic-induced weight gain) represent fundamentally different translational challenges, differing in effect size, biological complexity, and clinical readiness. We propose that the strategic integration of genome-wide analyses, sequencing, multi-omics data, and hypothesis-driven genetic studies may accelerate the clinical adoption of pharmacogenetics and contribute to more effective precision medicine in psychiatry.
By broadening gene discovery efforts to additional populations that have a disproportionately high risk of disease and leveraging genetic diversity in admixed populations, studies can identify population-enriched risk variants that traditionally have been missed in genome-wide association studies.
A. Horimoto, Nora Franceschini· HYPERTENSION· 0 citations
This review analyzes the use of WES as a strategic platform for personalized decision-making in contemporary practice given the multifactorial and heterogeneous complexity of AD, and proposes a hypothesis-generating theoretical framework whereby variants conventionally classified as benign or of uncertain significance...
Carlos Perezcano, M. Pérez-Coria, Ángel Ricardi-Mendoza· Life· 0 citations
How pharmacogenetics and pharmacogenomics function as enabling technologies across the pharmaceutical and clinical domains is synthesized, with emphasis on biomarker-guided drug development, patient stratification, safety optimization, regulatory translation, precision oncology, sex-related variability, population dive...
Nikolet Pavlova, D. Kaloudas, M. Traykovska et al.· Current Drug Discovery Techn...· 0 citations
WES is confirmed as a robust and scalable platform for population-level pharmacogenomic screening and broader clinical genomic applications, while demonstrating that haplotype-based imputation cannot fully overcome the intrinsic limitations of exome sequencing for comprehensive pharmacogenomic profiling.
A. Buianova, V. Cheranev, A. Shmitko et al.· Human Genomics· 0 citations
Assessment of several computational approaches using a dataset of pharmacogenomic variants with either clinical annotations or functional characterization by deep mutational scanning, with an additional focus on CYP2C9, a clinically relevant drug-metabolizing enzyme, indicates that computational models can complement i...
F. Pucci, Pauline Hermans, Matsvei Tsishyn et al.· bioRxiv· 0 citations
Background: Precision medicine increasingly relies on polygenic risk scores (PRS) to predict drug efficacy, safety, and therapeutic variability. Traditional monogenic pharmacogenetics, focused on individual gene variants, explains only 20-40% of drug response variation, leaving substantial "missing heritability." Polyg...
Irma Umar¹, Uzair Khalid², Sanwal Iqbal² et al.· Journal of Health, Wellness...· 0 citations
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