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Gustavo Ayala Department of Pathology and Laboratory Medicine, Dan L. Duncan Cancer Center, Department of Pathology and Immunology, Department of Veterans Affairs, University of Texas Health Sciences Center Medical School, Houston, Texas, USA

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Anna Frolov Department of Pathology and Laboratory Medicine, Dan L. Duncan Cancer Center, Department of Pathology and Immunology, Department of Veterans Affairs, University of Texas Health Sciences Center Medical School, Houston, Texas, USA
Department of Pathology and Laboratory Medicine, Dan L. Duncan Cancer Center, Department of Pathology and Immunology, Department of Veterans Affairs, University of Texas Health Sciences Center Medical School, Houston, Texas, USA

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Deyali Chatterjee Department of Pathology and Laboratory Medicine, Dan L. Duncan Cancer Center, Department of Pathology and Immunology, Department of Veterans Affairs, University of Texas Health Sciences Center Medical School, Houston, Texas, USA

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Dandan He Department of Pathology and Laboratory Medicine, Dan L. Duncan Cancer Center, Department of Pathology and Immunology, Department of Veterans Affairs, University of Texas Health Sciences Center Medical School, Houston, Texas, USA

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Susan Hilsenbeck Department of Pathology and Laboratory Medicine, Dan L. Duncan Cancer Center, Department of Pathology and Immunology, Department of Veterans Affairs, University of Texas Health Sciences Center Medical School, Houston, Texas, USA

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Michael Ittmann Department of Pathology and Laboratory Medicine, Dan L. Duncan Cancer Center, Department of Pathology and Immunology, Department of Veterans Affairs, University of Texas Health Sciences Center Medical School, Houston, Texas, USA
Department of Pathology and Laboratory Medicine, Dan L. Duncan Cancer Center, Department of Pathology and Immunology, Department of Veterans Affairs, University of Texas Health Sciences Center Medical School, Houston, Texas, USA

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particular the finding that the TMPRSS2/ERG (T/E) fusion gene is present in approximately 50% of prostate cancers. Results of experiments carried out on prostate cancer cells containing the T/E fusion ( Tomlins et al . 2005 ) indicate that the TMPRSS2

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-14-0586
Volume/Issue:
Volume 22: Issue 3
Free access
Matias Knuuttila Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland
Turku Center for Disease Modeling (TCDM), Institute of Biomedicine, University of Turku, Turku, Finland

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Arfa Mehmood Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland

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Jenni Mäki-Jouppila Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland
Turku Center for Disease Modeling (TCDM), Institute of Biomedicine, University of Turku, Turku, Finland

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Henrik Ryberg Center for Bone and Arthitis Research, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Pekka Taimen Department of Pathology, University of Turku and Turku University Hospital, Turku, Finland

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Juha Knaapila Department of Urology, Turku University Hospital, Turku, Finland

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Otto Ettala Department of Urology, Turku University Hospital, Turku, Finland

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Peter J Boström Department of Urology, Turku University Hospital, Turku, Finland

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Claes Ohlsson Center for Bone and Arthitis Research, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Mikko S Venäläinen Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland

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Asta Laiho Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland

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Laura L Elo Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland

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Petra Sipilä Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland
Turku Center for Disease Modeling (TCDM), Institute of Biomedicine, University of Turku, Turku, Finland

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Sari I Mäkelä Turku Center for Disease Modeling (TCDM), Institute of Biomedicine, University of Turku, Turku, Finland
Functional Foods Forum, University of Turku, Turku, Finland

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Matti Poutanen Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland
Turku Center for Disease Modeling (TCDM), Institute of Biomedicine, University of Turku, Turku, Finland
Center for Bone and Arthitis Research, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Refseq annotation. Immunohistochemistry To confirm the findings of RNA-seq analyses, the transmembrane protease, serine 2/ETS-related gene (TMPRSS2-ERG) fusion status in five tumors was studied with immunohistochemistry (IHC). In brief, sections

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-18-0148
Volume/Issue:
Volume 25: Issue 9
Free access
Charles E Massie Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Inmaculada Spiteri Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Helen Ross-Adams Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Hayley Luxton Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Jonathan Kay Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Hayley C Whitaker Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Mark J Dunning Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Alastair D Lamb Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK
Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK
Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Antonio Ramos-Montoya Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Daniel S Brewer Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Colin S Cooper Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK
Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Rosalind Eeles Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK
Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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UK Prostate ICGC Group
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Anne Y Warren Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Simon Tavaré Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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David E Neal Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK
Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK
Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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Andy G Lynch Cancer Research UK Cambridge Institute, Division of Genetics and Epidemiology, Department of Biological Sciences and School of Medicine, Royal Marsden NHS Foundation Trust, Departments of Pathology, Urology, Surgical Oncology, University of Cambridge, Cambridge, CB2 0RE, UK

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between the epigenetic silencing of HES5 and the expression of HES6 and provide evidence for interactions with known oncogenic pathways in prostate cancer (namely AR signalling and ERG gene fusions), highlighting a transcriptional network that is

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-14-0454
Volume/Issue:
Volume 22: Issue 2
Open access
Delila Gasi Tandefelt Departments of Pathology, Urology, Erasmus University Medical Centre, PO Box 2040, 2000 CA Rotterdam, The Netherlands

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Joost Boormans Departments of Pathology, Urology, Erasmus University Medical Centre, PO Box 2040, 2000 CA Rotterdam, The Netherlands

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Karin Hermans Departments of Pathology, Urology, Erasmus University Medical Centre, PO Box 2040, 2000 CA Rotterdam, The Netherlands

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Jan Trapman Departments of Pathology, Urology, Erasmus University Medical Centre, PO Box 2040, 2000 CA Rotterdam, The Netherlands

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-called Gleason grade ( Lotan & Epstein 2010 ). Similar to other tumors, prostate cancer growth is driven by the accumulation of genetic and epigenetic alterations. One of the earliest genetic alterations in prostate cancer is overexpression of the ERG oncogene

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-13-0390
Volume/Issue:
Volume 21: Issue 3
Free access
Xinyu Wu Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA

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Shiaoching Gong Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA
Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA

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Pradip Roy-Burman Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA

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Peng Lee Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA
Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA
Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA
Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA

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Zoran Culig Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA

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and the androgen receptor; contains AR splice variants Difficult to study TMPRSS2-ERG rearrangement in vitro due to the presence of wild-type TMPRSS2 and ERG genes CWR22 (Subline: CWR22Rv1, CWR-R1) Expresses PSA and AR. Growth is stimulated by

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-12-0285
Volume/Issue:
Volume 20: Issue 4
Free access
Ying Ying Sung Cancer Biology and Pharmacology, Genome Institute of Singapore, A*STAR (Agency for Science, Technology and Research), 60 Biopolis Street, #02-01 Genome, Singapore 138672, Singapore

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Edwin Cheung Cancer Biology and Pharmacology, Genome Institute of Singapore, A*STAR (Agency for Science, Technology and Research), 60 Biopolis Street, #02-01 Genome, Singapore 138672, Singapore

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of androgen dependence by ERG Chromosomal rearrangements between the regulatory region of the androgen-responsive gene TMPRSS2 and members of the ETS family of transcription factors such as ERG or ETV1 are commonly found in prostate cancers

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-13-0326
Volume/Issue:
Volume 21: Issue 1
Free access
Sangeeta Kumari Department of Cancer Biology, Cleveland Clinic, Cleveland, Ohio, USA

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Dhirodatta Senapati Department of Cancer Biology, Cleveland Clinic, Cleveland, Ohio, USA

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Hannelore V Heemers Department of Cancer Biology, Cleveland Clinic, Cleveland, Ohio, USA
Department of Urology, Cleveland Clinic, Cleveland, Ohio, USA
Department of Hematology/Medical Oncology, Cleveland Clinic, Cleveland, Ohio, USA

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-dependent transcription. ETS1 belongs to the same family of transcription factors as ERG. ERG’s function in CaP has become a hot topic since the identification of the TMPRSS2-ERG gene fusion, which has been linked to CaP cell invasion in preclinical models and to

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-17-0121
Volume/Issue:
Volume 24: Issue 8
Free access
Qu Deng Department of Epigenetics and Molecular Carcinogenesis, Program in Molecular Carcinogenesis, Cancer Stem Cell Institute, University of Texas MD Anderson Cancer Center, Science Park, Park Road 1C, Smithville, Texas 78957, USA
Department of Epigenetics and Molecular Carcinogenesis, Program in Molecular Carcinogenesis, Cancer Stem Cell Institute, University of Texas MD Anderson Cancer Center, Science Park, Park Road 1C, Smithville, Texas 78957, USA

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Dean G Tang Department of Epigenetics and Molecular Carcinogenesis, Program in Molecular Carcinogenesis, Cancer Stem Cell Institute, University of Texas MD Anderson Cancer Center, Science Park, Park Road 1C, Smithville, Texas 78957, USA
Department of Epigenetics and Molecular Carcinogenesis, Program in Molecular Carcinogenesis, Cancer Stem Cell Institute, University of Texas MD Anderson Cancer Center, Science Park, Park Road 1C, Smithville, Texas 78957, USA
Department of Epigenetics and Molecular Carcinogenesis, Program in Molecular Carcinogenesis, Cancer Stem Cell Institute, University of Texas MD Anderson Cancer Center, Science Park, Park Road 1C, Smithville, Texas 78957, USA

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regions could possess as many as ten genetic mutations ( Cooper et al . 2015 ). In untreated primary prostate cancer (PCa), genetic alterations such as TMPRSS2-ERG fusion and PTEN deletion within tumor clones could activate critical signaling pathways

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-15-0217
Volume/Issue:
Volume 22: Issue 6
Free access
Jamie L Van Etten Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA

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Scott M Dehm Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA
Department of Urology, University of Minnesota, Minneapolis, MN, USA

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evolution in response to selective pressures of therapy by targeted sequencing of plasma DNA and targeted deep sequencing of tumor biopsies obtained from patients with ERG-positive cancers ( Carreira et al . 2014 ). Together, these studies build upon an

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-16-0049
Volume/Issue:
Volume 23: Issue 4
Free access
Suzan Stelloo Division of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands

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Andries M Bergman Division of Oncogenomics, The Netherlands Cancer Institute, Amsterdam, The Netherlands
Division of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands

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Wilbert Zwart Division of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands
Department of Biomedical Engineering, Laboratory of Chemical Biology and Institute for Complex Molecular Systems, Eindhoven University of Technology, Eindhoven, The Netherlands

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) and AR-V7 splice variant ( Chen et al. 2018 ) ( Fig. 2C ), deeper mechanistic understanding of HOXB13 action in the AR signaling axis would be highly instrumental for designing novel therapeutics that would perturb this route. ERG fusions In

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-19-0032
Volume/Issue:
Volume 26: Issue 5
Free access