Genotyping of poor metabolisers of debrisoquine by allele-specific PCR amplification
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Cited by (537)
Pharmacogenomics
2020, Handbook of Analytical SeparationsCitation Excerpt :Each sample must be tested using both primers, and a PCR product will be generated only if a target sequence is present. In recent protocols, allele-specific assays have been developed to detect multiple variants, although typically two reactions must still be used in order to achieve adequate separation of the variants in the same position [28]. The use of fluorescent-based detection assays has improved significantly the specificity, detection limit, and stability of the allele-specific assay methods.
Prediction of drug response and adverse drug reactions: From twin studies to Next Generation Sequencing
2019, European Journal of Pharmaceutical SciencesCitation Excerpt :Similarly, in 1979 Michel Eichelbaum and colleagues published their findings that patients experiencing side-effects such as visual impairment, dizziness and headache following treatment with sparteine had excessive sparteine plasma concentrations and were homozygous for a genetic polymorphism in an autosomal locus, which later turned out to be CYP2D6 (Eichelbaum et al., 1979a; Eichelbaum et al., 1979b). The genetic locus underlying debrisoquine metabolism was elucidated 10–15 years later by Urs Meyer and Frank Gonzalez who identified the predominant CYP2D6 polymorphisms underlying poor metabolism (CYP2D6*3 and *4) (Gonzalez et al., 1988; Heim and Meyer, 1990), followed by the identification of CYP2D6 gene duplications as the molecular basis of ultrarapid metabolism (Johansson et al., 1993). Similar phenotype-driven approaches were used to identify polymorphisms responsible for differential activity of CYP2C9, CYP2C19 and CYP2A6.
Size-based separation methods of circulating tumor cells
2018, Advanced Drug Delivery ReviewsPolymorphic Variants of Cytochrome P450: Relevance to Cancer and Other Diseases
2015, Advances in PharmacologyCitation Excerpt :Soon after the study on debrisoquine metabolism in lung cancer patients, the CYP enzyme responsible for metabolism of debrisoquine and sparteine, now referred to as CYP2D6, was purified from human liver (Distlerath et al., 1985), followed by isolation of cDNA clones and mapping to chromosome 22 (Gonzalez et al., 1988). Subsequent genome mapping and cDNA sequencing enabled the identification of the main polymorphisms associated with absence of activity and development of genotyping assays to detect poor metabolizers (Daly, Armstrong, Monkman, Idle, & Idle, 1991; Gaedigk, Blum, Gaedigk, Eichelbaum, & Meyer, 1991; Gough et al., 1990; Hanioka, Kimura, Meyer, & Gonzalez, 1990; Heim & Meyer, 1990; Kagimoto, Heim, Kagimoto, Zeugin, & Meyer, 1990). These developments enabled the findings on lung cancer susceptibility obtained using debrisoquine phenotyping to be followed up in larger populations.
Explore the distribution of (rs35742686, rs3892097 and rs1065852) genetic polymorphisms of cytochrome P4502D6 gene in the Moroccan population
2022, Egyptian Journal of Medical Human Genetics