Figure 1
Figure 1. Lack of correlation of BCL2 SNP −938A>C with either BCL2 protein or mRNA levels in CLL. (A-C) Comparison of levels of BCL2 expression with −938A>C SNP. All 3 genotypes showed both low and high levels of BCL2 protein. β-actin was used as a standard for normalization of BCL2 expression, and then all samples were compared with levels observed in the cell line SC-1. For QRT-PCR, the samples were normalized to SC-1 RNA. The values represent the ratios of ΔΔCT SC-1 cell line to ΔΔCT patient RNA. Note that many of the patients with CLL with low BCL2 expression nevertheless expressed large amounts of BCL2 RNA. Arrows in top panels denote SNP −938C>A. (D) Range of levels of expression of BCL2 protein in 100 patients with CLL according to BCL2 promoter SNP −938 A>C. Horizontal bar denotes mean value for each group. There was no significant change in the levels of BCL2 protein expression with the SNP genotype. (E) Time to first treatment in the 98 patients from this cohort treated to date according to the BCL2 promoter SNP −938 A>C, showing lack of influence of the SNP in this series.

Lack of correlation of BCL2 SNP −938A>C with either BCL2 protein or mRNA levels in CLL. (A-C) Comparison of levels of BCL2 expression with −938A>C SNP. All 3 genotypes showed both low and high levels of BCL2 protein. β-actin was used as a standard for normalization of BCL2 expression, and then all samples were compared with levels observed in the cell line SC-1. For QRT-PCR, the samples were normalized to SC-1 RNA. The values represent the ratios of ΔΔCT SC-1 cell line to ΔΔCT patient RNA. Note that many of the patients with CLL with low BCL2 expression nevertheless expressed large amounts of BCL2 RNA. Arrows in top panels denote SNP −938C>A. (D) Range of levels of expression of BCL2 protein in 100 patients with CLL according to BCL2 promoter SNP −938 A>C. Horizontal bar denotes mean value for each group. There was no significant change in the levels of BCL2 protein expression with the SNP genotype. (E) Time to first treatment in the 98 patients from this cohort treated to date according to the BCL2 promoter SNP −938 A>C, showing lack of influence of the SNP in this series.

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