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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
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Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...
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Pharmacogenetics and pharmacogenomics examine how genetic factors influence an individual's response to drugs. While pharmacogenetics focuses on the impact of specific genetic variants on drug effects, pharmacogenomics takes a broader approach, studying how genetic variation across populations contributes to differences in drug responses. These fields aim to explain why individuals may experience varying levels of efficacy or adverse reactions to the same medication.Variability in drug...
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Genetic polymorphism in drug metabolism is crucial to the inter-individual variability observed in drug responses. Drug metabolism primarily involves the chemical modification of drugs and other xenobiotics to enhance their elimination by increasing their polarity. Two main classes of enzymes mediate this biotransformation process: Phase I enzymes, primarily cytochrome P450s, catalyze oxidation and reduction reactions, while other enzymes, such as esterases, mediate hydrolysis, and Phase II...
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The human genome is over 99.9% identical between individuals, yet genetic differences exist at millions of bases. The human genome contains approximately 3 million variant positions per individual, many of which are heterozygous, contributing to genetic diversity and individual traits. Genetic variations include single-nucleotide polymorphisms (SNPs), insertions, deletions, and copy number variations (CNVs).SNPs, the most common variation, involve single-base changes in DNA. These can be...
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Pharmacogenomics in acute lymphoblastic leukemia.

Shawn H R Lee1, Jun J Yang2

  • 1KTP-University Children's Medical Institute, National University Hospital, Singapore.

Best Practice & Research. Clinical Haematology
|October 21, 2017
PubMed
Summary

Pharmacogenomics advances personalized medicine for childhood acute lymphoblastic leukemia (ALL). Genetic factors are identified to tailor drug therapy, improving safety and effectiveness for better patient outcomes.

Keywords:
ALLAcuteLeukemiaLymphoblasticMRDPharmacogenomicsResponseToxicity

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Area of Science:

  • Pharmacogenomics
  • Personalized Medicine
  • Pediatric Oncology

Background:

  • Childhood acute lymphoblastic leukemia (ALL) is the most common pediatric malignancy.
  • Standardized clinical trials are used for ALL treatment.
  • Pharmacogenomics offers potential for tailored ALL therapy.

Purpose of the Study:

  • To review the role of pharmacogenomics in childhood ALL.
  • To identify germline genetic factors influencing drug response and toxicity in ALL patients.
  • To discuss the clinical utility and future directions of pharmacogenomic applications in ALL treatment.

Main Methods:

  • Review of genome-wide association studies (GWAS) and other genetic research in childhood ALL.
  • Analysis of identified germline variants affecting drug metabolism and toxicity.
  • Synthesis of evidence for clinical utility of genetic markers.

Main Results:

  • Multiple germline risk factors modifying drug response in ALL have been identified.
  • Specific genetic associations (e.g., TPMT, NUDT15) show clinical utility for mercaptopurine dosing.
  • Germline factors influencing susceptibility to adverse effects of other antileukemic agents are emerging.

Conclusions:

  • Pharmacogenomic discoveries are crucial for optimizing ALL treatment.
  • Clinical implementation of genetic tests (e.g., TPMT, NUDT15) can guide therapy adjustments.
  • Further research integrating germline and somatic variants is needed for precision pharmacotherapy in ALL.