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Related Concept Videos

Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
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...
Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...

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Related Experiment Video

Updated: May 26, 2026

Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
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Gene susceptibility to oxidative damage: from single nucleotide polymorphisms to function.

Valeria Simonelli1, Filomena Mazzei, Mariarosaria D'Errico

  • 1Department of Environment and Primary Prevention, Istituto Superiore di Sanità, Rome, Italy. valeria.simonelli@iss.it

Mutation Research
|December 14, 2011
PubMed
Summary

DNA repair of oxidative damage is crucial for cancer prevention. This review examines how common genetic variations (SNPs) in DNA repair proteins may influence cancer risk.

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Area of Science:

  • Biochemistry
  • Genetics
  • Oncology

Background:

  • Oxidative DNA damage can lead to mutations and cancer.
  • Germline mutations in DNA repair genes like MUTYH increase cancer risk.
  • The role of single nucleotide polymorphisms (SNPs) in sporadic cancer is less understood due to milder effects and study limitations.

Purpose of the Study:

  • To review common SNPs in oxidative DNA damage repair proteins.
  • To correlate biochemical/structural data with functional effects of these variants.
  • To assess the potential impact of SNPs on disease pathogenesis.

Main Methods:

  • Literature review focusing on common SNPs in oxidative DNA damage repair proteins.
  • Analysis of biochemical and structural data for repair proteins.
  • Evaluation of functional effects and disease association studies.

Main Results:

  • The review synthesizes information on well-studied SNPs.
  • It highlights the challenges in accurately assessing functional impacts and epidemiological links.
  • It bridges molecular data with potential clinical relevance.

Conclusions:

  • Understanding SNPs in DNA repair proteins is vital for assessing cancer risk.
  • Further research with robust assays and study designs is needed.
  • This review provides a foundation for future investigations into SNP-mediated cancer pathogenesis.