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CYP2D6 phenotype-genotype relationships in African-Americans and Caucasians in Los Angeles.

机译：CYP2D6表型-基因型关系在洛杉矶的非洲裔美国人和高加索人中。

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CYP2D6 genotyping (CYP2D6*3, CYP2D6*4, CYP2D6*5, CYP2D6*13, CYP2D6*16 alleles and gene duplications) was previously performed on 1053 Caucasian and African-American lung cancer cases and control individuals and no significant difference in allele frequencies between cases and control individuals detected. We have carried out additional genotyping (CYP2D6*6, CYP2D6*7, CYP2D6*8, CYP2D6*9, CYP2D6*10, CYP2D6*17 alleles) and debrisoquine phenotyping on subgroups from this study to assess phenotype-genotype relationships. African-Americans showed significant differences from Caucasians with respect to frequency of defective CYP2D6 alleles, particularly CYP2D6*4 and CYP2D6*5. The CYP2D6*17 allele occurred at a frequency of 0.26 among 87 African-Americans and appeared to explain higher average metabolic ratios among African-Americans compared with Caucasians. CYP2D6*6, CYP2D6*8, CYP2D6*9 and CYP2D6*10 were rare in both ethnic groups but explained approximately 40% of higher than expected metabolic ratios among extensive metabolizers. Among individuals phenotyped with debrisoquine, 32 out of 359 were in the poor metabolizer range with 24 of these (75%) also showing two defective CYP2D6 alleles. Additional single strand conformational polymorphism analysis screening of samples showing large phenotype-genotype discrepancies resulted in the detection of three novel polymorphisms. If subjects taking potentially interfering drugs were excluded, this additional screening enabled the positive identification of 88% of phenotypic poor metabolizers by genotyping. This sensitivity was comparable with that of phenotyping, which identified 90% of those with two defective alleles as poor metabolizers.
机译：CYP2D6基因分型（CYP2D6 * 3，CYP2D6 * 4，CYP2D6 * 5，CYP2D6 * 13，CYP2D6 * 16等位基因和基因重复）先前在1053名白种人和非洲裔美国人肺癌病例和对照个体中进行，等位基因频率无显着差异病例和对照个体之间发现。我们对本研究的亚组进行了额外的基因分型（CYP2D6 * 6，CYP2D6 * 7，CYP2D6 * 8，CYP2D6 * 9，CYP2D6 * 10，CYP2D6 * 17等位基因）和去氢异喹酮表型分析，以评估表型与基因型之间的关系。在有缺陷的CYP2D6等位基因，特别是CYP2D6 * 4和CYP2D6 * 5的频率上，非裔美国人与白种人表现出显着差异。 CYP2D6 * 17等位基因在87位非裔美国人中的发生频率为0.26，似乎解释了与高加索人相比非裔美国人平均代谢率更高。 CYP2D6 * 6，CYP2D6 * 8，CYP2D6 * 9和CYP2D6 * 10在这两个族裔中均很少见，但解释了广泛代谢者中约40％的代谢率高于预期。在用地溴异喹定型的个体中，359个个体中有32个处于弱代谢者范围，其中24个个体（75％）还显示出两个缺陷的CYP2D6等位基因。对表现出大的表型-基因型差异的样品进行额外的单链构象多态性分析筛选，结果发现了三种新的多态性。如果排除服用潜在干扰药物的受试者，则通过基因分型，这种额外的筛查可以对88％的表型不良代谢者进行阳性鉴定。这种敏感性与表型相当，后者将具有两个缺陷等位基因的人中的90％鉴定为不良代谢者。

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