Abstract

You have accessJournal of UrologyProstate Cancer: Basic Research & Pathophysiology IV1 Apr 2016MP90-05 PROSTATE CANCER GENE EXPRESSION SIGNATURES ASSOCIATED WITH CAPSULE AND SEMINAL VESICLE INVASION AND BIOCHEMICAL RECURRENCE AFTER RADICAL PROSTATECTOMY Travis Allemang, Michael Williams, Shilpa Katta, Gyorgy Petrovics, Inger Rosner, and Albert Dobi Travis AllemangTravis Allemang More articles by this author , Michael WilliamsMichael Williams More articles by this author , Shilpa KattaShilpa Katta More articles by this author , Gyorgy PetrovicsGyorgy Petrovics More articles by this author , Inger RosnerInger Rosner More articles by this author , and Albert DobiAlbert Dobi More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2016.02.2549AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Major strides in oncologic treatment and prognostication have occurred by insights into cancer gene expression signatures. The goal of this study was to identify prostate cancer gene expression signatures associated with extra capsular extension, seminal vesicle invasion, and biochemical recurrence (BCR). METHODS Gene expression microarray data from 40 Caucasian men who underwent radical prostatectomy was analyzed from the publicly available NCBI Gene Expression Omnibus GSE32448 developed by the CPDR. Groups analyzed were based on final pathologic stage pT3a and pT3b disease, as well as those with negative surgical margins which developed BCR following radical prostatectomy. Gene expression signatures for each group were identified using bioinformatics analysis. Signatures were then applied to Genomatix© software for defining key regulatory nodes. Further comparison was made to the gene panels utilized in the commercially available ProlarisTM, Oncotype DX Genomic Prostate ScoreTM, and DecipherTM. RESULTS There was a median follow-up of 15.5 years post prostatectomy. Those with pT3a disease were found to have 182 unique gene signatures of which 83 of the genes were found to have biological functions to include cell migration, locomotion or regulation of epithelial cell proliferation (p <0.0001). Those with pT3b disease were found to have 1569 unique gene signatures compared to subjects with pT3a disease. These genes were found to be associated with cellular functions to include protein targeting and localization, RNA processing and cell cycle (p<0.001). Genes unique to the development of BCR include down regulation of VEGF-A and the HLA gene family as key regulatory nodes. The genes unique to the absence of BCR include upregulation of ERG and downregulation of ETS. Compared to the commercially available gene panels, subjects with pT3b disease shared 13 unique genes with these gene panels. Among those with BCR only 1 gene was uniquely shared with the commercially available gene panels. CONCLUSIONS These results suggest that unique gene expression signatures exist at the time of prostatectomy which are associated with pT3a, pT3b disease, and BCR. Among the commercially available gene panels, these products were found to have genes which correlated predominantly with advanced pathologic disease and had little correlation with BCR among this cohort. Future work is warranted to validate the expression of these unique genes as they could serve to compliment current prognostic approaches. © 2016FiguresReferencesRelatedDetails Volume 195Issue 4SApril 2016Page: e1146 Advertisement Copyright & Permissions© 2016MetricsAuthor Information Travis Allemang More articles by this author Michael Williams More articles by this author Shilpa Katta More articles by this author Gyorgy Petrovics More articles by this author Inger Rosner More articles by this author Albert Dobi More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.