ID

45164

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Principal Investigator: Mark A. Rubin, Weill Cornell Medical College, New York, NY, USA MeSH: Prostatic Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000310 Half of prostate cancers harbor gene fusions between *TMPRSS2* and members of the *ETS* transcription factor family. To date little is known about the presence of non-ETS fusion events in prostate cancer. We employed next-generation transcriptome sequencing (RNA-Seq) in order to explore the whole transcriptome of 25 human prostate cancer samples for the presence of chimeric fusion transcripts. We generated more than 1 billion sequence reads and used a novel computational approach (FusionSeq) in order to identify novel gene fusion candidates with high confidence. In total, we discovered and characterized seven new cancer-specific gene fusions, two involving the ETS genes *ETV1* and *ERG*, and five involving non-ETS genes such as *CDKN1A* (p21), *CD9* and *IKBKB* (IKK-beta), genes known to exhibit key biological roles in cellular homeostasis or assumed to be critical in tumorigenesis of other tumor entities, as well as the oncogene PIGU and the tumor suppressor gene *RSRC2*. The novel gene fusions are found to be of low frequency but interestingly, the non-ETS fusions were all present in prostate cancer harboring the *TMPRSS2-ERG* gene fusion. Future work will focus on determining if the ETS rearrangements in prostate cancer are associated or directly predispose to a rearrangement prone phenotype.

Link

dbGaP study = phs000310

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Versions (2)

1. 8/25/22 8/25/22 - Simon Heim
2. 10/12/22 10/12/22 - Adrian Schulz

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Mark A. Rubin, Weill Cornell Medical College, New York, NY, USA

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October 12, 2022

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