Purpose Tamoxifen showed individual differences in efficacy under different CYP2D6*10 genotypes. Our study evaluated the prognosis of tamoxifen or toremifene in hormone receptor (HR)–positive breast cancer patients under different genotypes.
Materials and Methods CYP2D6*10 genotypes of HR-positive breast cancer patients were determined by Sanger sequencing, and all the patients were divided into tamoxifen group or toremifene group.
Results A total of 268 patients with HR-positive breast cancer were studied. The median follow-up time was 72.0 months (range, 5.0 to 88.0 months). Of these, 88 (32.9%), 114 (42.5%), and 66 (24.6%) patients had C/C, C/T, and T/T genotypes, respectively. Among patients who received tamoxifen (n=176), the 5-year disease-free survival (DFS) rate in patients with C/C and C/T genotype was better than that in patients with T/T genotype, and the difference was statistically significant (p < 0.001 and p=0.030, respectively). In patients receiving toremifene, CYP2D6*10 genotype was not significantly associated with DFS (p=0.325). Regardless of genotypes, the 5-year DFS rate was higher in patients treated with toremifene than in patients with tamoxifen (91.3% vs. 80.0%, p=0.011). Compared with tamoxifen, toremifene remained an independent prognostic marker of DFS in multivariate analysis (hazard ratio, 0.422; p=0.021). For all the 180 patients with CYP2D6*10 C/T and T/T genotypes, the 5-year DFS rate was significantly higher in the toremifene group than in the tamoxifen group (90.8% vs. 70.1%, p=0.003).
Conclusion Toremifene may be an alternative adjuvant endocrine therapy for patients with CYP2D6*10 mutant genotypes.
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PURPOSE Many of the enzymes handling environmental factors are polymorphic and may confer variable susceptibility to renal cell carcinoma (RCC). Among those, the author studied genetic polymorphisms of CYP2D6 (B & T) and CYP1A1 in RCCs and controls in Korean. MATERIALS AND METHODS Using 132 RCCs and 94 controls, first PCR products were obtained in 104 RCCs and 94 controls with CYP2D6, and 74 RCCs and 56 controls with CYP1A1. Res triction enzyme - BstN I/EcoN I for CYP2D6 (B & T), and NCo I for CYP1A1-digestion was followed to analyze constitutive DNA. RESULTS In both RCCs and controls, no mutant allele of CYP2D6 (B & T) was detected and the susceptibility for occurrence of RCC was unable to evaluate. With CYP1A1 RFLP, homozy gous wild type (WW) was seen in 68 (52.3%; 37 RCCs, 31 controls), heterozygous mutant type (WM) in 54 (41.5%; 32 RCCs, 22 controls) and homozygous mutant type (MM) in 8 (6.2%; 5 RCCs, 3 controls). The odds ratios (95% CI) of RCC susceptibility for CYP1A1 genotype were 1.15 for WM and 1.36 for MM. Even though not significant statistically, higher tendency in MM presented. CONCLUSION There is no association between susceptibility for the occurrence of RCC and genetic polymorphism of CYP2D6 (B & T) and CYP1A1.