Genomic DNA was extracted from peripheral blood taken on EDTA from 92 AML patients and 135 healthy individuals using a Qiagen DNA Isolation Kit (QIAGEN, Hilden, Germany). DNA was also isolated from AML cell lines. DNA purity and concentration were verified on the DeNovix DS-11 spectrophotometer (DeNovix Inc., Wilmington, DE, USA). Isolated DNA was subsequently stored at −20 °C until further use.
BSG and MCT1 SNPs were selected based on three criteria: (1) minor allele frequency (MAF) in European populations higher than 0.15, (2) a functional effect on expression/protein structure predicted by the National Institute of Environmental Health Sciences SNP Function Prediction tool [36 (link)], and (3) lack of high linkage disequilibrium between the SNPs. Based on these criteria, six SNPs (four in the gene coding for BSG and two in the gene coding for MCT1) were chosen. BSG and MCT1 SNP were determined using TaqMan SNP Genotyping (Applied Biosystems, Waltham, MA, USA) and LightSNiP (TIB MOLBIOL, Berlin, Germany) assays. PCR was performed on a LightCycler 480 II (Roche Diagnostics, Rotkreuz, Switzerland) according to the manufacturers’ protocols.
BSG and MCT1 SNPs were selected based on three criteria: (1) minor allele frequency (MAF) in European populations higher than 0.15, (2) a functional effect on expression/protein structure predicted by the National Institute of Environmental Health Sciences SNP Function Prediction tool [36 (link)], and (3) lack of high linkage disequilibrium between the SNPs. Based on these criteria, six SNPs (four in the gene coding for BSG and two in the gene coding for MCT1) were chosen. BSG and MCT1 SNP were determined using TaqMan SNP Genotyping (Applied Biosystems, Waltham, MA, USA) and LightSNiP (TIB MOLBIOL, Berlin, Germany) assays. PCR was performed on a LightCycler 480 II (Roche Diagnostics, Rotkreuz, Switzerland) according to the manufacturers’ protocols.
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