Scott Dehm
@scottdehm
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Professor @UMNcancer studying steroid hormones, androgen receptors, and #ProstateCancer genomes. Apogee Enterprises Chair in Cancer Research . Views=mine.
Minneapolis, MN
Joined May 2011
RT @AarmstrongDuke: Can anyone top the Halabi model for predicting survival in mCRPC? Yes! Dr Halabi does it again! See our ctDNA based cli….
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RT @JakeOrmeMDPhD: Fascinating work by Chen et al in uncovering new metabolomics of SPOP-mutant prostate cancer, we review here @EAntonarak….
nature.com
Nature Cancer - CHD1 loss is common in SPOP-mutant prostate cancer; however, this combined phenotype has not yet been clearly defined. Genetically engineered mouse models of prostate cancer with...
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RT @LukeSelth: Check out our new work exploring AR biology in advanced prostate cancer: We found that tumours expr….
eu-focus.europeanurology.com
The androgen receptor (AR) is a master regulator in prostate cancer, but the relevance of its truncated variants remains unclear. Using patient-derived models, we demonstrated that expression of the...
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RT @ProstateCell: 🧪 Dr. @scottdehm and collaborators including @huang_lab, @EAntonarakis, & @mishabeltran showed that double-negative #CRPC….
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@UMNCancer @UMN_GradSchool This study benefitted from tremendous collaborations with @huang_lab @EAntonarakis @mishabeltran @JoshLangMD @AttardLab and many others!.
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This work was led by a talented graduate student (Sam Pitzen) @umncancer @UMN_GradSchool who will soon be defending his PhD thesis (and entering the job market).
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KLF5 was identified as the transcription factor that supports these transcriptional features. Defining DNPC by what "it is" (a hybrid basal/club/hillock phenotype), instead of what "it's not" (negative for AR and neuroendocrine features) may aid development of new therapies.
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We found that the double-negative phenotype of castration-resistant prostate cancer (a.k.a. "DNPC") exhibits the same transcriptional features that define basal, club, and hillock epithelial cells of the benign prostate.
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Check out our latest study! Comparative transcriptomics reveals a mixed basal, club, and hillock epithelial cell identity in castration-resistant prostate cancer | PNAS
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RT @JoshLangMD: Thrilled to share a project that we envisioned over a decade ago to perform high purity/high specificity molecular analysis….
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Excited to share a new paper by postdoc Dr. Kiel Tietz @UMNCancer! CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells: Cell Reports . Work funded by @CDMRP and @NCICancerBio.
cell.com
Tietz et al. report that CPSF1 is upregulated in patients with advanced prostate cancer and that the knockdown of CPSF1 inhibits prostate cancer growth and glycolytic output. Knockdown of CPSF1...
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RT @mishabeltran: In memory of Dr. Felix Feng. Thank you @EUplatinum for honoring our beloved colleague and friend, gone too soon. We miss….
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RT @EAntonarakis: The two faces of FOXA1 muts in PCa. Congrats to Justin Hwang for this revised classification of FOXA1 alts in PCa. Differ….
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RT @DrChoueiri: PROSTATE Paper 2.Franseschini et al. developed a targeted DNA methylation assay for the detection of neuroendocrine prostat….
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RT @DrChoueiri: It is this time of the Year again: 10 TOP TRANSLATIONAL PAPERS IN GU ONCOLOGY!. 1/ Prostate Paper 1.Fonseca et al. introdu….
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RT @DrChoueiri: PROSTATE Paper 3.Knutson et al. developed the AR-ctDETECT assay to detect ctDNA in limiting plasma cfDNA from pts w/ #mCRPC….
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RT @APCCC_Lugano: AR alterations inform circulating tumor DNA detection in metastatic castration resistant prostate cancer patients out in….
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@AarmstrongDuke @DukeCancer @DukeGUCancer @theNCI @PCFnews We thank all the contributors to this collaborative study! @UMNCancer @mishabeltran @charlesryanmd @EAntonarakis @lukegaughan22.
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This study was a collaboration initiated with .@AarmstrongDuke and Susan Halabi .@DukeCancer @DukeGUCancer and was funded by .@theNCI and @PCFnews!.
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Our paper out today in @NatureComms analyzed plasma from the phase 3 @ALLIANCE_org A031201 trial using the AR-ctDETECT assay. Patients positive for circulating tumor DNA had poor overall survival despite treatment with potent AR inhibitors.
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