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Cytogenetic biomarkers and genetic polymorphisms.

Hannu Norppa1

  • 1Laboratory of Molecular and Cellular Toxicology, Department of Industrial Hygiene and Toxicology, Finnish Institute of Occupational Health, FIN-00250 Helsinki, Finland. hannu.norppa@ttl.fi

Toxicology Letters
|April 20, 2004
PubMed
Summary

Chromosomal aberrations (CAs) predict cancer risk, unlike sister chromatid exchanges (SCEs) or micronuclei (MN). Genetic variations in detoxification and DNA repair influence these biomarkers and cancer susceptibility, even in non-smokers.

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Area of Science:

  • Environmental Health Sciences
  • Toxicology
  • Genetic Epidemiology

Background:

  • Cytogenetic biomarkers like chromosomal aberrations (CAs), sister chromatid exchanges (SCEs), and micronuclei (MN) are used to monitor genotoxic exposure and early cancer development.
  • International studies have investigated the predictive value of elevated biomarker levels in lymphocytes for cancer risk.

Purpose of the Study:

  • To evaluate the association between cytogenetic biomarkers and cancer risk.
  • To explore the role of individual susceptibility factors, including genetic polymorphisms, in modulating these associations.

Main Methods:

  • Analysis of chromosomal aberrations (CAs), sister chromatid exchanges (SCEs), and micronuclei (MN) in peripheral lymphocytes.
  • Investigation of genetic polymorphisms in xenobiotic-metabolizing enzymes (e.g., GSTM1, GSTT1, NAT2), DNA repair genes (e.g., XRCC1, XPD), and folate metabolism (e.g., MTHFR, MTRR).

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  • Correlation of biomarker levels and genotypes with cancer risk, considering factors like smoking and occupational exposure.

    • Main Results:

    • Elevated CAs, but not SCEs or MN, were found to be predictive of cancer risk.
    • This CA-cancer association was independent of exposure timing, smoking, or occupational exposures, and was observed in unexposed non-smokers.
    • Specific genotypes, such as the glutathione S-transferase M1 (GSTM1) null genotype, were linked to increased sensitivity to genotoxicity and higher CA/SCE frequencies.
    • Polymorphisms in NAT2, GSTT1, XRCC1, XPD, MTHFR, and MTRR were also associated with baseline levels of CAs, SCEs, or MN, suggesting a role in detoxifying or repairing genotoxic damage.

    Conclusions:

    • Chromosomal aberrations are a significant predictor of cancer risk, potentially indicating individual susceptibility.
    • Genetic polymorphisms in metabolic, DNA repair, and folate pathways play a crucial role in modulating genotoxic effects and cancer susceptibility.
    • Further research into these genetic factors can refine risk assessment and identify individuals at higher risk.