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Fresh Look at Gene Fusion Yields Clues in Low-Risk Prostate Cancer

Gina Battaglia, PhD
Published: Wednesday, Jan 10, 2018
John C. Cheville, MD

John C. Cheville, MD
Although gene fusions between the TMPRSS2 gene and ETS family of transcription factors (most commonly the ERG gene) in prostate cancer have been recognized for more than a decade, the clinical relevance of this fusion event continues to be debated among experts. However, the findings of a recent study suggests that the mechanism through which this fusion occurs may be more important than the presence of the fusion for identifying low-risk prostate cancers, since retention of the interstitial genes between the TMPRSS2 and ERG genes post fusion occurred more frequently in prostate cancers classified as very low or low risk.1

Knowledge About Fusion Event

Fusion between the TMPRSS2 gene and the ETS transcription family is thought to be an early event that occurs in approximately half of all prostate cancers, although the mechanisms for this fusion are not completely clear. ETS family members are involved in the regulation of cell growth, proliferation, differentiation, and apoptosis via activation or repression of its target genes. In prostate cancer, the positioning of androgen-responsive promotors in frame is thought to initiate overexpression of the members of the ETS family. For example, the androgen-responsive gene TMPRSS2 is fused near its first exon with its promoter in frame with the 5’ exons of the ERG gene, which retains the characteristic functional domains of the ETS family.
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