Saturday, October 8, 2011

ERG, the partner in the TMPRSS2-ERG fusion, is frequently methylated in prostate cancer

From the Alumkal lab at OHSU, comes the paper

A DNA methylation microarray-based study identifies ERG as a gene commonly methylated in prostate cancer 
Bascially, ERG is normally repressed in CaP in absence of the TMPRSS2-ERG fusion -- where it is upregulated by virtue of the TMPRSS2 promoter -- this report describes the findings from a methylation array, showing that 74% of prostate tumors are methylated at ERG.  This is interesting as the argument to date has been that TMPRSS2-driven ERG expression is a bad player in prostate cancer -- but if ERG is repressed by methylation specifically in the tumors, that would suggest inactivation of ERG is a bad player.  Do these two expression states of ERG define biologically distinct tumor types?  Can both events occur simultaneously - one allele forming the fusion and one that is methylated?  Is ERG activation or inactivation not so important because neither event actually drives tumorigenesis or progression?  read all about it if you have access to Epigenetics (link above)!

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