We suspect that our analysis comparing CIC-ERF co-deletion to CIC-ERF WT tumors did not reach statistical significance due to the inability to identify other prostate tumors that have increased ETV1 expression from alternative mechanisms, beyond CIC-ERF co-deletions.
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The <i>CIC-ERF</i> co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression.
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