Pharmacogenomics for Precision Medicine, 2nd Edition

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 25 November 2026 | Viewed by 1224

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Institute of Cardiology, Medical Academy, Lithuanian University of Health Sciences, Sukilėlių g. 15, LT-50009 Kaunas, Lithuania
Interests: pharmacogenomics; cardiovascular disease; blood coagulation; antiplatelets; anticoagulants; statins; metabolomics
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Special Issue Information

Dear Colleagues,

Pharmacogenomics is an advanced approach to tailoring medications to individual patients based on their unique genetic makeup. Rather than relying on a one-size-fits-all approach, this technique considers individual variability. While genetic, epigenetic, and gene-expression variability were once believed to be independent factors of phenotype variation, recent studies have shown that they work in tandem to produce distinct effects of medication on an individual.

In addition to host-related factors, researchers are increasingly recognizing that pathogens (such as bacteria) can also contribute to treatment variability. Variations in pathogen genetics, mutation rates, and interaction with the host's body can influence how effectively medications work for each patient. Therefore, the interaction between host genomic factors and pathogen traits is a key part of understanding pharmacogenomics and treatment outcomes.

Although research has highlighted the significance of these combined factors in drug effects, the widespread use of pharmacogenomics data remains uncommon in many countries. This may be due to several factors, such as researchers' inconsistent interpretation of data or difficulties in understanding and applying these results to precision medicine.

This Special Issue invites new research articles that demonstrate the use of pharmacogenomics knowledge in clinical practice (e.g., as part of precision medicine), present economic evaluations of drugs or methods used in therapy, and describe innovative approaches to educating clinical personnel and high school students about pharmacogenomics and precise treatment.

Dr. Vacis Tatarūnas
Guest Editor

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Keywords

  • pharmacogenomics in precise therapy
  • tailored medicine
  • pharmacoeconomics
  • personalized medicine
  • education in pharmacogenomics and precise medicine
  • future directions in pharmacogenomics
  • pharmacogenomics and phenotype
  • host-bacteria interaction in pharmacogenomics
  • genotype, epigenetic variation, and gene expression axis in pharmacogenomics

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Related Special Issue

Published Papers (2 papers)

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Research

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16 pages, 725 KB  
Article
Clinical and Biomarker Predictors of Adverse Left Ventricular Remodeling After First STEMI: Insights into Phenotype Variability Using CMR
by Agneta Virbickiene, Vacis Tatarunas, Ieva Ciapiene, Neda Jonaitiene, Justina Jureviciute, Paulius Bucius, Arnoldas Leleika, Ieva Jonauskiene, Liepa Kleizaite, Tomas Lapinskas and Olivija Dobiliene
Pharmaceuticals 2026, 19(5), 794; https://doi.org/10.3390/ph19050794 - 19 May 2026
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Abstract
Background: Adverse left ventricular remodeling (ALVR) remains an important complication after ST-segment elevation myocardial infarction (STEMI) despite timely reperfusion therapy. Early circulating biomarkers reflecting thromboinflammatory and eicosanoid-related pathways may improve identification of patients at risk of unfavorable remodeling. Objectives: To investigate whether platelet [...] Read more.
Background: Adverse left ventricular remodeling (ALVR) remains an important complication after ST-segment elevation myocardial infarction (STEMI) despite timely reperfusion therapy. Early circulating biomarkers reflecting thromboinflammatory and eicosanoid-related pathways may improve identification of patients at risk of unfavorable remodeling. Objectives: To investigate whether platelet count, 20-hydroxyeicosatetraenoic acid (20-HETE), 15(S)-hydroxyeicosatetraenoic acid [15(S)-HETE], and NETosis activity measured on the morning after reperfusion therapy are associated with serial cardiac magnetic resonance (CMR)-defined ALVR after first STEMI. Methods: In this prospective single-center study, 93 patients with first STEMI treated with reperfusion therapy, including primary percutaneous coronary intervention (PCI) in 87 patients and thrombolysis followed by PCI underwent baseline CMR at a median of 4 days after PCI and repeat CMR at 6 months. ALVR was defined as a ≥12% increase in both left ventricular end-diastolic volume and left ventricular end-systolic volume at follow-up. Fasting blood samples obtained on the morning after PCI were used to measure platelet count, 20-HETE, 15(S)-HETE, and NETosis activity. Univariable and multivariable logistic regression and receiver operating characteristic analyses were performed. A secondary exploratory analysis evaluated predictors of absolute improvement in left ventricular ejection fraction (LVEF) of ≥10%. Results: ALVR occurred in 19 of 93 patients (20.4%). Patients with ALVR had lower platelet count and lower 20-HETE levels at baseline. In the multivariable model, lower platelet count (OR 0.981, 95% CI 0.965–0.996; p = 0.015) and lower 20-HETE (OR 0.985, 95% CI 0.970–1.000; p = 0.047) were independently associated with ALVR, whereas urea was not significant. In receiver operating characteristic analysis, 20-HETE showed the highest discriminatory ability for ALVR (AUC 0.713, 95% CI 0.594–0.833; p < 0.001), followed by platelet count (AUC 0.670, 95% CI 0.546–0.794; p = 0.007). By contrast, 15(S)-HETE and NETosis activity were not significant discriminators in the primary analyses. Overall LV function improved during follow-up, with LVEF increasing from 49.0% to 56.0% (p < 0.001). In secondary exploratory analysis, higher HDL was independently associated with LVEF improvement of ≥10% (OR 7.84, 95% CI 1.26–48.99; p = 0.028). Conclusions: Lower platelet count and lower 20-HETE measured on the morning after PCI were independently associated with subsequent CMR-defined ALVR after first STEMI. Platelet count may serve as a simple, clinically accessible marker of risk, while 20-HETE suggests a potential role of eicosanoid-related pathways in remodeling process. Full article
(This article belongs to the Special Issue Pharmacogenomics for Precision Medicine, 2nd Edition)
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Review

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27 pages, 2712 KB  
Review
Pharmacogenomic Stratification for Oncology Drug Repurposing: An Exposure Target Context Eligibility Framework
by Mohamed El-Tanani, Adil Farooq Wali, Syed Arman Rabbani, Yahia El-Tanani, Imran Rangraze and Frezah Muhana
Pharmaceuticals 2026, 19(6), 957; https://doi.org/10.3390/ph19060957 - 19 Jun 2026
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Abstract
In spite of plausible biology, the majority of oncology trials involving drug repurposing have failed to demonstrate any efficacy. Numerous factors can potentially cause failure, including issues with dosing, drug strength, the trial design itself, and patient diversity. A major, potentially correctable contributor [...] Read more.
In spite of plausible biology, the majority of oncology trials involving drug repurposing have failed to demonstrate any efficacy. Numerous factors can potentially cause failure, including issues with dosing, drug strength, the trial design itself, and patient diversity. A major, potentially correctable contributor is the absence of pharmacogenomic eligibility criteria. Here, we propose the Pharmacogenomic Stratification Framework for Drug Repurposing (PSDR), a novel framework for drug response that encompasses the triad of Exposure (E, pharmacokinetic adequacy), Target engagement (T, somatic tumor genomics), and Context competence (C, tumor microenvironment). These domains are represented as R = E × T × C, an eligibility model capturing the necessary, though not sufficient, conditions for anticancer drug activity. The model is not presented as an empirically validated quantitative law but as a conceptual framework to guide biomarker-stratified trial design. We derive five testable pharmacogenomic hypotheses for metformin, statins, beta-blockers, NSAIDs, and SSRIs, and propose a three-point PSDR eligibility scoring system. Prospective validation of each hypothesis in appropriately stratified cohorts is required before clinical implementation. The PSDR framework complements rather than replaces existing precision oncology resources (OncoKB, CIViC, PharmGKB, CPIC, DepMap, GDSC) by integrating germline pharmacokinetics, somatic genomics, and microenvironmental profiling for repurposed agents. If validated, PSDR-guided enrichment designs could substantially improve the efficiency and interpretability of repurposing trials. The PSDR framework should be considered a conceptual and hypothesis-generating model that requires prospective validation before clinical implementation. Full article
(This article belongs to the Special Issue Pharmacogenomics for Precision Medicine, 2nd Edition)
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