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Xi Wei Department of Diagnostic and Therapeutic Ultrasonography, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China

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Shang Cai Department of Oncology, Southern Research Institute and Cancer Cell Biology Program, the University of Alabama at Birmingham Comprehensive Cancer Center, Birmingham, Alabama, USA
Department of Radiotherapy and Oncology, the Second Affiliated Hospital of Soochow University, Suzhou, China

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Rebecca J Boohaker Department of Oncology, Southern Research Institute and Cancer Cell Biology Program, the University of Alabama at Birmingham Comprehensive Cancer Center, Birmingham, Alabama, USA

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Joshua Fried Department of Oncology, Southern Research Institute and Cancer Cell Biology Program, the University of Alabama at Birmingham Comprehensive Cancer Center, Birmingham, Alabama, USA

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Ying Li The Third Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China

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Linfei Hu Department of Thyroid Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China

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Yi Pan Department of Thyroid Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China

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Ruifen Cheng Department of Thyroid Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China

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Sheng Zhang Department of Diagnostic and Therapeutic Ultrasonography, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China

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Ye Tian Department of Radiotherapy and Oncology, the Second Affiliated Hospital of Soochow University, Suzhou, China

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Ming Gao Department of Thyroid Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China

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Bo Xu Department of Oncology, Southern Research Institute and Cancer Cell Biology Program, the University of Alabama at Birmingham Comprehensive Cancer Center, Birmingham, Alabama, USA
Department of Molecular Radiation Oncology, Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China

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overexpression and poor clinical prognosis. KAT5 promotes ATC cell invasion and proliferation through acetylating C-MYC, thus inhibiting ubiquitination proteasome degradation and stabilizing the protein. Furthermore, we demonstrate evidence that overexpression of

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-18-0193
Volume/Issue:
Volume 26: Issue 1
Free access
D J Liao Vincent T Lombardi Cancer Center, Georgetown University Medical Center, Washington DC 20007, USA.

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R B Dickson Vincent T Lombardi Cancer Center, Georgetown University Medical Center, Washington DC 20007, USA.

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Ever since Bishop and his co-workers discovered the c-myc gene in the late 1970s (Bishop 1982), voluminous literature has documented its central role in proliferation and malignant transformation of human and animal cells (Amati et al. 1998, Bouchard et al. 1998, Dang et al. 1999). Most, if not all, types of human malignancy have been reported to have amplification and/or overexpression of this gene, although the frequency of these alterations varies greatly among different reports (Nesbit et al. 1999). In 1992, researchers started to realize that aberrant expression of c-myc could cause apoptosis (Evan et al. 1992, Shi et al. 1992), although the phenomenon had actually been observed much earlier (Wurm et al. 1986). Studies in recent years have further shown that the c-myc gene regulates growth, both in the sense of cell size and in the context of tissue differentiation (Gandarillas & Watt 1997, Iritani & Eisenman 1999, Johnston et al. 1999, Schmidt 1999, Schuhmacher et al. 1999). Thus, it is now known that the c-myc gene participates in most aspects of cellular function, including replication, growth, metabolism, differentiation, and apoptosis (Packham & Cleveland 1995, Hoffman & Liebermann 1998, Dang 1999, Dang et al. 1999, Elend & Eilers 1999, Prendergast 1999). How the c-Myc protein may be specifically directed to perform one, but not the others, of these functions is still obscure, despite the fact that the relevant literature has been accumulating at a fast pace in the past two decades. This review focuses on the profound roles of c-Myc in breast cancer and in the actions of the hormones that are eitologically related to breast cancer.

Article Type:
Abstract
Volume/Issue:
Volume 7: Issue 3
Free access
Maya Dadiani Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel

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Dalia Seger Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel

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Tamar Kreizman Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel

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Daria Badikhi Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel

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Raanan Margalit Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel

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Raya Eilam Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel

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Hadassa Degani Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel

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’ regulator in breast cancer is the c-Myc proto-oncogene that encodes the c-Myc transcription factor. Estrogen has been shown to activate c-Myc expression in ERα-positive human breast cancer cells through its enhanced transcription ( Dubik & Shiu 1988

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-08-0249
Volume/Issue:
Volume 16: Issue 3
Free access
Alison J Butt
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Catriona M McNeil
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Elizabeth A Musgrove
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Robert L Sutherland
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increased c-Myc expression, which occurs within 15 min of oestrogen stimulation ( Dubik et al. 1987 , Dubik & Shiu 1988 ). The DNA binding region of ERα is required for c-Myc induction, and the P2 promoter region of the MYC gene contains an atypical ERE

Article Type:
Research Article
DOI:
https://doi.org/10.1677/erc.1.00993
Volume/Issue:
Volume 12: Issue Supplement_1
Free access
D Dworakowska Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK
Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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E Wlodek Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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C A Leontiou Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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S Igreja Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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M Cakir Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK
Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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M Teng Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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N Prodromou Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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M I Góth Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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S Grozinsky-Glasberg Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK
Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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M Gueorguiev Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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B Kola Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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M Korbonits Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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A B Grossman Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK

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phosphorylate ERK1 and ERK2 at two sites, Tyr185 followed by Thr183 ( Haystead et al . 1992 ). ERK1/2 in turn phosphorylates and activates ribosomal S6 kinase and transcription factors such as c-MYC, Elk1, c-Fos or CYCLIN D1 ( Terada et al . 1999 a , b

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-09-0101
Volume/Issue:
Volume 16: Issue 4
Free access
Gina Chia-Yi Chu Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Haiyen E Zhau Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Ruoxiang Wang Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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André Rogatko Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Xu Feng Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Majd Zayzafoon Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Youhua Liu Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Mary C Farach-Carson Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Sungyong You Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Jayoung Kim Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Michael R Freeman Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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Leland W K Chung Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of
Uro-Oncology Research, Surgery, Biomedical Sciences, Biostatistics and Bioinformatics Center, Department of Pathology, Department of Pathology, Department of Biochemistry and Cell Biology, Department of Medicine, Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, 8750 Beverly Blvd., Atrium 103, Los Angeles, California 90048, USA Departments of

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downstream c-Myc/Max or c-Met signaling network abolished skeletal metastasis in mice. Animal models also showed that RANKL-expressing PCa cells conferred bone colonizing and aggressive phenotypes to neighboring non-metastatic bystander cells by activating

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-13-0548
Volume/Issue:
Volume 21: Issue 2
Open access
Salma Kaochar Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Dan L. Duncan Comprehensive Cancer Center, Houston, Texas, USA
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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Aleksandra Rusin Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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Christopher Foley Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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Kimal Rajapakshe Dan L. Duncan Comprehensive Cancer Center, Houston, Texas, USA
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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Matthew Robertson Dan L. Duncan Comprehensive Cancer Center, Houston, Texas, USA
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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Darlene Skapura Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

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Cammy Mason Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

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Karen Berman De Ruiz Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

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Alexey Mikhailovich Tyryshkin Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

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Jenny Deng Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

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Jin Na Shin Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

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Warren Fiskus Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

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Jianrong Dong Dan L. Duncan Comprehensive Cancer Center, Houston, Texas, USA
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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Shixia Huang Dan L. Duncan Comprehensive Cancer Center, Houston, Texas, USA
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA
Department of Education, Innovation, and Technology, Baylor College of Medicine, Houston, Texas, USA

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Nora M Navone Division of Cancer Medicine, Department of Genitourinary Medical Oncology, The University of Texas Anderson Cancer Center, Houston, Texas, USA

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Christel M Davis Avera Institute for Human Genetics, Sioux Falls, South Dakota, USA

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Erik A Ehli Avera Institute for Human Genetics, Sioux Falls, South Dakota, USA

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Cristian Coarfa Dan L. Duncan Comprehensive Cancer Center, Houston, Texas, USA
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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Nicholas Mitsiades Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Dan L. Duncan Comprehensive Cancer Center, Houston, Texas, USA
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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inhibit the GATA2 transcriptional program. Dilazep suppressed the expression of AR, c-MYC, FOXM1, CENPF, EZH2, and several other PC drivers. Using cellular thermal shift assay (CETSA), ChIP-qPCR, and GATA2 DNA-binding assay, we further confirmed GATA2

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-21-0085
Volume/Issue:
Volume 29: Issue 1
Open access
Céline Van Themsche Research Group in Molecular Oncology and Endocrinology, Department of Chemistry and Biology, Canada Research Chair in Molecular Gyneco-Oncology, Université du Québec à Trois-Rivières, 3351, Boul. des Forges, CP 500, Trois-Rivières, Québec, Canada G9A 5H7

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Sophie Parent Research Group in Molecular Oncology and Endocrinology, Department of Chemistry and Biology, Canada Research Chair in Molecular Gyneco-Oncology, Université du Québec à Trois-Rivières, 3351, Boul. des Forges, CP 500, Trois-Rivières, Québec, Canada G9A 5H7

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Valérie Leblanc Research Group in Molecular Oncology and Endocrinology, Department of Chemistry and Biology, Canada Research Chair in Molecular Gyneco-Oncology, Université du Québec à Trois-Rivières, 3351, Boul. des Forges, CP 500, Trois-Rivières, Québec, Canada G9A 5H7

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Caroline Descôteaux Research Group in Molecular Oncology and Endocrinology, Department of Chemistry and Biology, Canada Research Chair in Molecular Gyneco-Oncology, Université du Québec à Trois-Rivières, 3351, Boul. des Forges, CP 500, Trois-Rivières, Québec, Canada G9A 5H7

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Anne-Marie Simard Research Group in Molecular Oncology and Endocrinology, Department of Chemistry and Biology, Canada Research Chair in Molecular Gyneco-Oncology, Université du Québec à Trois-Rivières, 3351, Boul. des Forges, CP 500, Trois-Rivières, Québec, Canada G9A 5H7

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Gervais Bérubé Research Group in Molecular Oncology and Endocrinology, Department of Chemistry and Biology, Canada Research Chair in Molecular Gyneco-Oncology, Université du Québec à Trois-Rivières, 3351, Boul. des Forges, CP 500, Trois-Rivières, Québec, Canada G9A 5H7

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Eric Asselin Research Group in Molecular Oncology and Endocrinology, Department of Chemistry and Biology, Canada Research Chair in Molecular Gyneco-Oncology, Université du Québec à Trois-Rivières, 3351, Boul. des Forges, CP 500, Trois-Rivières, Québec, Canada G9A 5H7

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′ (antisense) for c- myc ; 5′-CGGGCTTCAACGCAGACTA-3′ (sense) and 5′-GGTCCGTGCAGAAGTCCTG-3′ (antisense) for c- fos ; 5′-CAATGGCCACCATGGAGAAC-3′ (sense) and 5′-AACGGTGTCGTCGAAACAGC-3′ (antisense) for tff1 ; 5′-GTCAGTGGTGGACCTGACCT-3′ (sense) and 5

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-09-0113
Volume/Issue:
Volume 16: Issue 4
Free access
Stefan J Barfeld Prostate Cancer Research Group Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, N-0318 Oslo, Norway

Department of Cancer Prevention Institute of Cancer Research

Department of Urology Oslo University Hospital, N-0424 Oslo, Norway

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Harri M Itkonen Prostate Cancer Research Group Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, N-0318 Oslo, Norway

Department of Cancer Prevention Institute of Cancer Research

Department of Urology Oslo University Hospital, N-0424 Oslo, Norway

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Alfonso Urbanucci Prostate Cancer Research Group Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, N-0318 Oslo, Norway

Department of Cancer Prevention Institute of Cancer Research

Department of Urology Oslo University Hospital, N-0424 Oslo, Norway

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Ian G Mills Prostate Cancer Research Group Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, N-0318 Oslo, Norway

Department of Cancer Prevention Institute of Cancer Research

Department of Urology Oslo University Hospital, N-0424 Oslo, Norway
Prostate Cancer Research Group Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, N-0318 Oslo, Norway

Department of Cancer Prevention Institute of Cancer Research

Department of Urology Oslo University Hospital, N-0424 Oslo, Norway
Prostate Cancer Research Group Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, N-0318 Oslo, Norway

Department of Cancer Prevention Institute of Cancer Research

Department of Urology Oslo University Hospital, N-0424 Oslo, Norway

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, including c-Myc, which is overexpressed and predictive of poor prognosis in a subset of cases ( Hawksworth et al . 2010 ). Other examples include hypoxia-inducible factor 1α (HIF1A), which is associated with PCa metastasis ( Ranasinghe et al . 2013 ). In

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-13-0515
Volume/Issue:
Volume 21: Issue 4
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W-D Han
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Y-L Zhao
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Y-G Meng
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L Zang
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Z-Q Wu
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Q Li
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Y-L Si
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K Huang
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J-M Ba
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H Morinaga
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M Nomura
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Y-M Mu
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Cruz, Biotechnology, Santa Cruz, CA, USA), and c-Myc (Invitrogen) were used in this study. All immunoblotting procedures were performed as described ( Han et al. 2003 ). Protein–protein interaction assays in cell-free (GST

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-06-0082
Volume/Issue:
Volume 14: Issue 3
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