ArticleOncogene2008
TMPRSS2-ERG fusion, a common genomic alteration in prostate cancer activates C-MYC and abrogates prostate epithelial differentiation.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
149 citing papers in PubMed, 3 syntheses or guidelines pooled it, 247 citations in OpenAlex.
- The role of microRNA in castration-resistant prostate cancer.Urologic oncology · 2014Pooled it
- Loss of the NKX3.1 tumorsuppressor promotes the TMPRSS2-ERG fusion gene expression in prostate cancer.BMC cancer · 2014Pooled it
- Prevalence and clinical application ofAsian journal of andrologyPooled it
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- A ligandable PNT domain establishes ERG as a directly targetable oncogenic driver in prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- TMPRSS2-ERG confers resistance of prostate cancer to antiandrogens.EMBO molecular medicine · 2026Article
- Review
- ERG expression is not predictive of outcome in patients with intermediate- and high-risk localized prostate cancer treated with combined androgen blockade and radiotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Oncogenic Fusions HarboringCancers · 2025Review
- Bridging Cancer and COVID-19: The Complex Interplay of ACE2 and TMPRSS2.Cancer medicine · 2025Review
- Mechanism-centric regulatory network identifies NME2 and MYC programs as markers of Enzalutamide resistance in CRPC.Nature communications · 2024Article
- The Androgen Receptor Does Not Directly Regulate the Transcription of DNA Damage Response Genes.Molecular cancer research : MCR · 2023Article
- TMPRSS2-ERG promotes the initiation of prostate cancer by suppressing oncogene-induced senescence.Cancer gene therapy · 2022Article
- Characterization of stage-specific tumor progression in TMPRSS2-ERG (fusion)-driven and non-fusion-driven prostate cancer in GEM models.Molecular carcinogenesis · 2022Article
- Comparative Pathobiology of Canine and Human Prostate Cancer: State of the Art and Future Directions.Cancers · 2022Review
- The Expression of Proto-OncogeneInternational journal of molecular sciences · 2022Review
- Review
- Article
- New Selective Inhibitors of ERG Positive Prostate Cancer: ERGi-USU-6 Salt Derivatives.ACS medicinal chemistry letters · 2021Article
- MEX3D is an oncogenic driver in prostate cancer.The Prostate · 2021Article
89 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 5 institutions in 1 country.
Funding
Abstract
The high prevalence of TMPRSS2-ERG rearrangements ( approximately 60%) in prostate cancer (CaP) leads to androgenic induction of the ETS-related gene (ERG) expression. However, the biological functions of ERG overexpression in CaP remain to be understood. ERG knockdown in TMPRSS2-ERG expressing CaP cells induced striking morphological changes and inhibited cell growth both in cell culture and SCID mice. Evaluation of the transcriptome and specific gene promoters in ERG siRNA-treated cells and investigation of gene expression signatures of human prostate tumors revealed ERG-mediated activation of C-MYC oncogene and the repression of prostate epithelial differentiation genes (PSA and SLC45A3/Prostein). Taken together, these data combining cell culture and animal models and human prostate tumors reveal that ERG overexpression in prostate tumor cells may contribute to the neoplastic process by activating C-MYC and by abrogating prostate epithelial differentiation as indicated by prostate epithelial specific markers.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.