Genetic polymorphism and variability of chemical carcinogenesis

Biochemistry (Mosc). 2008 May;73(5):543-54. doi: 10.1134/s0006297908050076.

Abstract

Risk assessment in chemical carcinogenesis involves ratios of several factors. Individual responses of an organism to carcinogenic agents depend on polymorphism of enzymes responsible for metabolic activation/detoxification of carcinogens, DNA repair, and apoptosis, as well as promotion and progression in malignantly transformed cells. The effects of a particular polymorphic variant are manifested only in the case of its high penetrance. An integral effect is formed by the ratio of procarcinogenic and anticarcinogenic effects. The complexity of risk assessment depends on the gene polymorphism mosaic involved, directly or indirectly, in tumorigenesis and upstream/downstream interactions of gene products.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Carcinogens / chemistry
  • Carcinogens / toxicity*
  • Cell Transformation, Neoplastic / drug effects*
  • Cell Transformation, Neoplastic / genetics*
  • Cytochrome P-450 Enzyme System / genetics
  • Cytochrome P-450 Enzyme System / metabolism
  • DNA Repair Enzymes / genetics
  • DNA Repair Enzymes / metabolism
  • Humans
  • Mutagens / chemistry
  • Mutagens / toxicity
  • Polymorphism, Genetic*

Substances

  • Carcinogens
  • Mutagens
  • Cytochrome P-450 Enzyme System
  • DNA Repair Enzymes