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L line BCM1, the expression of both genes is opposite: no levels of MAGE-A1 [2^(Ct) 1.07] and high levelsof BORIS [2^(Ct) 24.39]. We transiently transfected expression plasmid encoding BORIS into both cell lines, with negligible transcript levels of MAGE-A1, and quantified endogenous MAGE-A1 mRNA by RT (reverse transcription)-PCR and gel electrophoresis. As depicted in Figure 1, BORIS was able to

L line BCM1, the expression of both genes is opposite: no levels of MAGE-A1 [2^(Ct) 1.07] and high levelsof BORIS [2^(Ct) 24.39]. We transiently transfected expression plasmid encoding BORIS into both cell lines, with negligible transcript levels of MAGE-A1, and quantified endogenous MAGE-A1 mRNA by RT (reverse transcription)-PCR and gel electrophoresis. As depicted in Figure 1, BORIS was able to

Activate the MAGE-A1 promoter and to which extent, we compared its influence with the stimulatory effect of 5-aza-CdR and/or TSA on MAGE-A1 transcription in cancer cell line settings. For our current investigations, we chose 3 breast cancer cell lines: MDA-MB-468, MCF-7 and BCM1 because of their different levels of MAGE-A1 and BORIS transcripts. As shown in Table 1 and measured by quantitative rea

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Activate the MAGE-A1 promoter and to which extent, we compared its influence with the stimulatory effect of 5-aza-CdR and/or TSA on MAGE-A1 transcription in cancer cell line settings. For our current investigations, we chose 3 breast cancer cell lines: MDA-MB-468, MCF-7 and BCM1 because of their different levels of MAGE-A1 and BORIS transcripts. As shown in Table 1 and measured by quantitative rea

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