Abstract
In this study, we have quantified the mRNA expression levels of multidrug resistance gene 1 (MDR1) in the normal kidney cortex and renal cell carcinoma (RCC) segments from 24 Japanese nephrectomized patients by real-time polymerase chain reaction (PCR). The mRNA expression level of MDR1 in RCC segments was significantly decreased in comparison with each normal segment (P=0.0042, by Student’s paired t-test). In addition, the ten common single nucleotide polymorphisms (SNPs) of the MDR1 gene in the patients were assessed using the PCR-restriction enzyme fragment length polymorphism method to investigate the influence of these SNPs on its mRNA expression levels. The allele frequencies of these SNPs were comparable with our previous report in the Japanese recipients of living-donor liver transplantation (Goto et al., Pharmacogenetics 12:451–457; 2002). MDR1 expression levels in the normal kidney cortex were independent on the five SNPs, which were polymorphic in the Japanese population. Furthermore, the effect of the SNPs on expression levels of MDR1 mRNA in RCC segments was not recognized. These findings suggest that the common SNPs in the MDR1 gene have no influence on the expression of its transcript in RCC segments as well as in the normal kidney cortex.
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Acknowledgements
This work was supported by a grant-in-aid for Research on Human Genome, Tissue Engineering, and Food Biotechnology from the Ministry of Health, Labor, and Welfare of Japan (H12-Genome-019), a grant-in-aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan, and the 21st Century COE Program “Knowledge Information Infrastructure for Genome Science”. M.G. is supported as a Research Assistant by the 21st Century COE Program “Knowledge Information Infrastructure for Genome Science”.
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Uwai, Y., Masuda, S., Goto, M. et al. Common single nucleotide polymorphisms of the MDR1 gene have no influence on its mRNA expression level of normal kidney cortex and renal cell carcinoma in Japanese nephrectomized patients. J Hum Genet 49, 40–45 (2004). https://doi.org/10.1007/s10038-003-0105-4
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DOI: https://doi.org/10.1007/s10038-003-0105-4
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