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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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Pharmacogenomics: Identification of New Drug Targets01:29

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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: Overview01:29

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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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Pharmacogenetics of Drug Metabolism: Overview01:27

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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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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
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Pharmacogenomics for leukemia treatment.

Yoichi Tanaka1

  • 1Department of Clinical Pharmacy, Center for Clinical Pharmacy and Sciences, School of Pharmacy, Kitasato University.

[Rinsho Ketsueki] the Japanese Journal of Clinical Hematology
|August 9, 2016
PubMed
Summary

Genetic variations significantly impact drug responses in children with acute lymphoblastic leukemia. NUDT15 gene variants, not TPMT, are key predictors of thiopurine drug effectiveness in Japanese patients.

Area of Science:

  • Pharmacogenomics
  • Oncology
  • Genetics

Background:

  • Individual responses to drugs like 6-mercaptopurine (6-MP) vary due to genetic factors.
  • Standard genetic tests like TPMT are less effective for Japanese populations in predicting 6-MP response.
  • NUDT15 polymorphisms show promise for predicting thiopurine therapy outcomes in Asian populations.

Purpose of the Study:

  • To investigate the relationship between genetic variants and therapeutic responses in Japanese children with acute lymphoblastic leukemia.
  • To determine if genetic factors identified in Western populations are applicable to Japanese patients.
  • To establish a basis for personalized thiopurine therapy in this demographic.

Main Methods:

  • Analysis of genetic variants (polymorphisms) in Japanese childhood acute lymphoblastic leukemia patients.

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  • Correlation of specific genetic variants with patient sensitivity and response to thiopurine drugs.
  • Comparison of genetic variant frequencies and their impact across different racial groups.

    • Main Results:

    • TPMT deficiency is infrequent in Japanese patients, limiting its utility for predicting 6-MP response.
    • NUDT15 polymorphisms are identified as significant predictors of thiopurine therapy responsiveness in the studied population.
    • Genetic differences necessitate race-specific investigations for pharmacogenomic applications.

    Conclusions:

    • NUDT15 genetic variants are crucial for personalizing thiopurine treatment in Japanese children with acute lymphoblastic leukemia.
    • Race-specific pharmacogenomic data are essential for effective personalized medicine.
    • Further research is needed to fully elucidate the role of genetic factors in optimizing cancer therapy.