[Genetic polymorphisms and cancer risk]

Gan To Kagaku Ryoho. 2004 Jun;31(6):853-7.
[Article in Japanese]

Abstract

While hereditary disease genes have a high lifelong cumulative incidence rate (penetrance), the penetrance for polymorphism genotypes is not high. Polymorphisms relating to cancer incidence are classified into 1. carcinogen metabolizing enzymes (CYPs, GSTs, NQO1, etc.), 2. DNA repair enzymes (OGG1, XRCC1, XPD, etc.), 3. DNA synthesis and methylation (MTHFR, MS, etc.), 4. cytokines and inflammation-related enzymes (IL-1B, TNF-A, MPO, etc.), and 5. sex hormone metabolizing enzymes and the receptors (CYP19, SRD5A2, ER, etc.). Since genotypes cannot be manipulated, they are not the factors subject to prevention. However, the finding that the strength of association between lifestyle and disease occurrence is influenced by genotypes (gene-environment interaction), opens the door to genotype applications for disease prevention practice.

Publication types

  • Review

MeSH terms

  • Cytochrome P-450 CYP1A1 / genetics
  • Cytochrome P-450 CYP1A1 / metabolism
  • DNA Glycosylases / metabolism
  • DNA Repair
  • Genetic Predisposition to Disease*
  • Genotype
  • Glutathione Transferase / metabolism
  • Humans
  • Interleukins / genetics
  • Neoplasms / enzymology
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Polymorphism, Genetic*
  • Risk Factors
  • Steroid 17-alpha-Hydroxylase / genetics

Substances

  • Interleukins
  • Cytochrome P-450 CYP1A1
  • Steroid 17-alpha-Hydroxylase
  • Glutathione Transferase
  • glutathione S-transferase M1
  • DNA Glycosylases
  • oxoguanine glycosylase 1, human