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Fig. 5B ; .54, 55 These sequence changes result in a striking reduction in the quantity of TPMT, 54 probably because the variant protein is degraded rapidly.56 A series of less frequent TPMT variant alleles have also been described.51 Finally, there are large differences in the types and frequencies of TPMT alleles among ethnic groups. For example, TPMT * 3A, the most common allele responsible for very low levels of enzyme activity in whites, with a frequency of approximately 4 percent Fig. 5B ; , has not been observed in China, Korea, or Japan.57 Other examples of pharmacogenetic variation involving phase II pathways of drug metabolism are listed in Table 2. Recurring themes in pharmacogenetics include the presence of a few relatively common variant alleles of genes encoding proteins important in drug response, a larger number of much less frequent variant alleles, and striking differences in the types and frequencies of alleles among different populations and ethnic groups. These generalizations, based primarily on studies of drug metabolism, are now being extended to include common genetic variations in other proteins that might alter the effects of drug transporters or targets. Most drugs are metabolized by several different enzymes, can be transported by other types of proteins, and ultimately interact with one or more targets. If several steps in this type of pathway were to display genetic variation -- that is, if the effects were polygenic -- clear multimodal frequency distributions like those shown in Figures 2 and 3 would quickly be replaced by multiple overlapping distributions. Therefore, even if inheritance influenced the effect of a drug, the relatively simple, oneto-one relation observed for CYP2D6 and TPMT.
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