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Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

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...
Principles of Pharmacogenetics: Types of Genetic Variants01:27

Principles of Pharmacogenetics: Types of Genetic Variants

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...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

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...
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...

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Related Experiment Video

Updated: Jun 26, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Platinum neurotoxicity pharmacogenetics.

Sarah R McWhinney1, Richard M Goldberg, Howard L McLeod

  • 1School of Pharmacy, Institute for Pharmacogenomics and Individualized Therapy, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, Campus Box 7360, 3203 Kerr Hall, Chapel Hill, NC 27599-7360, USA.

Molecular Cancer Therapeutics
|January 14, 2009
PubMed
Summary

Platinum-based chemotherapy drugs like cisplatin can cause debilitating neurotoxicity. This review explores genetic markers to predict and potentially prevent this severe side effect in cancer patients.

Related Experiment Videos

Last Updated: Jun 26, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Area of Science:

  • Oncology
  • Pharmacology
  • Genetics

Background:

  • Platinum-based chemotherapy agents (cisplatin, carboplatin, oxaliplatin) are vital in treating various cancers.
  • Severe neurotoxicity is a significant dose-limiting side effect, often leading to treatment discontinuation and reduced patient benefit.
  • Current methods to prevent platinum-induced neurotoxicity have been largely unsuccessful.

Purpose of the Study:

  • To review current literature on genetic markers associated with platinum chemotherapy-induced neurotoxicity.
  • To identify potential biomarkers for predicting and managing neurotoxicity.
  • To explore the development of mechanism-based toxicity modulators.

Main Methods:

  • Systematic review of existing research on genetic associations with neurotoxicity from platinum agents.
  • Analysis of data from single-agent and combination platinum chemotherapy studies.
  • Focus on identifying genetic variations linked to platinum-induced peripheral neuropathy and other neurotoxic effects.

Main Results:

  • Genetic markers show potential in predicting individual susceptibility to platinum-induced neurotoxicity.
  • Certain genetic variations are associated with increased risk of developing severe neurotoxic side effects.
  • Understanding these associations is crucial for personalized treatment strategies.

Conclusions:

  • Genetic biomarkers offer a promising avenue for predicting and potentially mitigating platinum chemotherapy-induced neurotoxicity.
  • Further research into mechanism-based associations could lead to novel therapeutic strategies to improve patient outcomes.
  • Developing targeted interventions based on genetic profiles may enhance the tolerability of essential platinum-based cancer treatments.