Abstract
Inter-individual variability in carcinogen metabolism has been attributed in part to the polymorphic expression of several phase I and II detoxification enzymes. The role of these genetic polymorphisms in cancer susceptibility has been most extensively evaluated for isozymes of cytochrome P450 (CYP1A1, CYP2D6, and CYP2E1), N-acetyltransferase (NAT1 and NAT2), glutathione S-transferase (GSTM1, GSTT1, and GSTP1), microsomal epoxide hydrolase, and NAD(P)H:quinone oxidoreductase. Our understanding of the genetic basis of cancer risk has been enhanced most recently by establishment of genotype-phenotype correlations in humans and identification of numerous diverse factors, both genetic and environmental, that can modify risk.
| Original language | English |
|---|---|
| Pages (from-to) | 251-256 |
| Number of pages | 6 |
| Journal | Current Oncology Reports |
| Volume | 2 |
| Issue number | 3 |
| DOIs | |
| State | Published - May 2000 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
-
SDG 3 Good Health and Well-being
Keywords
- Female
- Genetic Predisposition to Disease/epidemiology
- Genetic Testing
- Humans
- Male
- Neoplasms/epidemiology
- Polymorphism, Genetic
- Risk Assessment
- Risk Factors
- Sensitivity and Specificity
Fingerprint
Dive into the research topics of 'Genetic polymorphism and cancer risk.'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver