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The differential expression pattern of the BMI-1, SALL4 and ABCA3 genes in myeloid leukemia

DOI: 10.1186/1475-2867-12-42

Keywords: SALL4 gene, BMI-1 gene, Real-time PCR, AML, CML

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Abstract:

Overexpression of the BMI-1 gene was found in the AML, CML-CP and CML-BC groups as compared with HI group, while the BMI-1 expression level was lower in patients who achieved CR. In contrast, significantly increased SALL4 expression was only found in AML group, additionally, SALL4 expression was lower in the CML-CP and CML-CR groups compared with the HI group, while the SALL4 expression level in the CML-BC group was higher and significantly greater than that in the CML-CP and CML-CR groups. Moreover, a positive correlation between the expression of SALL4 and BMI-1 genes was found in samples from most groups. There was no significant difference of ABCA3 expression level in AML and CML-BC group in comparison with HI group. Interestingly, the ABCA3 expression level was significantly decreased in the CML-CP, AML-CR and CML-CR in comparison with the HI group. Moreover, the ABCA3 expression level in all of the CR groups was lower than that in their corresponding groups.These results describe the altered SALL4, ABCA3 and BMI-1 expression pattern in different phases of myeloid leukemia, which may relate to the development and progression to different diseases. SALL4 expression was strongly correlated with BMI-1 in most of the myeloid leukemia patient groups, providing a potential link between SALL4 and BMI-1 in leukemogenesis.The altered expression of genes, such as WT1, SCL, and Notch1, that play crucial roles in the regulation of hematopoietic progenitor cell proliferation is frequently found in leukemia [1-7]. Increasing data show that the genes involved in hematopoietic stem/progenitor cell (HSPC) proliferation change their expression pattern during leukemogenesis [8].SALL4 (sal-like protein 4), a SALL gene family member that is a newly identified zinc-finger transcription factor, was originally cloned based on its sequence homology to Drosophila spalt (sal) [9-12]. Alternative splicing generates two variant forms of human SALL4 mRNA, SALL4A and SALL4B, and each has a d

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