Genetic Polymorphisms of Xenobiotics-Metabolizing Enzymes Contributing to Leukemia

Abstract

Polymorphisms in xenobiotic-metabolizing enzymes have been linked to an increased risk of developing leukemia (XMEs). XMEs are found in all higher organisms and are one of the first lines of defense against environmental chemicals. Toxins, including therapeutic agents, are completely metabolized and eliminated from the body by an enzyme system that is encoded by specific genes. The majority of these genes are polymorphic, and some of the polymorphic forms have altered enzyme activity. Phase I XMEs, such as cytochrome P450s (CYPs), and phase II biotransformation enzymes, such as glutathione S-transferases (GST), UDP-glucuronosyltransferases (UGT), and N-acetyltransferases (NAT), are the most important. The majority of genetic variation discovered during clinical testing is due to single-nucleotide polymorphisms (SNPs). The purpose of this chapter is to highlight information about of some genetic polymorphisms of XMEs, contributing to AML, ALL, CML, and ALL. Several keywords were used to search the databases PubMed, Google Scholar, and Web of Science. Currently, numerous manuscripts suggested that genetic polymorphisms of XMEs were associated with ALL, CLL AML, and CML susceptibility.