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G Schlossmacher Faculty of Life Sciences, Faculty of Medical and Human Sciences, Centre for Endocrinology and Diabetes

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E Platt Faculty of Life Sciences, Faculty of Medical and Human Sciences, Centre for Endocrinology and Diabetes

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A Davies Faculty of Life Sciences, Faculty of Medical and Human Sciences, Centre for Endocrinology and Diabetes

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S Meredith Faculty of Life Sciences, Faculty of Medical and Human Sciences, Centre for Endocrinology and Diabetes

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A White Faculty of Life Sciences, Faculty of Medical and Human Sciences, Centre for Endocrinology and Diabetes
Faculty of Life Sciences, Faculty of Medical and Human Sciences, Centre for Endocrinology and Diabetes

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induce cell death by apoptosis in SCLC cells both in vitro ( Sommer et al . 2007 ) and in vivo in a xenograft model ( Sommer et al . 2010 ). In lymphoid cells, Gcs can induce marked apoptosis; hence, they are used for the treatment of haematological

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-13-0402
Volume/Issue:
Volume 20: Issue 6
Free access
Thomas A Werner Department of Surgery (A), Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Inga Nolten Department of Surgery (A), Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Levent Dizdar Department of Surgery (A), Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Jasmin C Riemer Institute of Pathology, Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Sina C Schütte Department of Surgery (A), Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Pablo E Verde Coordination Centre for Clinical Trials, Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Katharina Raba Institute for Transplantation Diagnostics and Cell Therapeutics, Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Matthias Schott Division of Endocrinology, Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Wolfram T Knoefel Department of Surgery (A), Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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Andreas Krieg Department of Surgery (A), Heinrich-Heine-University and University Hospital Duesseldorf, Duesseldorf, Germany

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-going high demand for the identification of relevant signalling pathways that influence the tumours biology and can be used to effectively target FTC. In this regard, TNF-related apoptosis-inducing ligand (TRAIL) and its receptors have gained considerable

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-17-0479
Volume/Issue:
Volume 25: Issue 3
Free access
Giuseppe Palladino Medical Oncology Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy

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Tiziana Notarangelo Laboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, Rionero in Vulture, Potenza, Italy

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Giuseppe Pannone Anatomic Pathology Unit, Department of Clinic and Experimental Medicine, University of Foggia, Foggia, Italy

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Annamaria Piscazzi Medical Oncology Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy

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Olga Lamacchia Endocrinology Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy

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Lorenza Sisinni Laboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, Rionero in Vulture, Potenza, Italy

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Girolamo Spagnoletti Medical Oncology Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy

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Paolo Toti Pathology Unit, Department of Human Pathology and Oncology, University of Siena, Siena, Italy

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Angela Santoro Institute of Histopathology and Diagnostic Cytopathology, Fondazione di Ricerca e Cura ‘Giovanni Paolo II’ UCSC, Campobasso, Italy

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Giovanni Storto Nuclear Medicine Unit, IRCCS, Referral Cancer Center of Basilicata, Rionero in Vulture, Potenza, Italy

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Pantaleo Bufo Anatomic Pathology Unit, Department of Clinic and Experimental Medicine, University of Foggia, Foggia, Italy

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Mauro Cignarelli Endocrinology Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy

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Franca Esposito Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, Naples, Italy

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Matteo Landriscina Medical Oncology Unit, Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy
Laboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, Rionero in Vulture, Potenza, Italy

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apoptosis-resistant phenotypes ( Nikiforov et al. 2011 ). Therefore, several attempts have been made to study the molecular mechanisms responsible for the more aggressive phenotype of radioiodine-refractory thyroid tumors with the aim to find molecular

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-16-0063
Volume/Issue:
Volume 23: Issue 9
Free access
Yan Zhou Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Invasion and Metastasis Research, Institute of Cancer Research, Capital Medical University, Beijing, China

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Gaoxiang Yang Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Invasion and Metastasis Research, Institute of Cancer Research, Capital Medical University, Beijing, China

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Hua Tian Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Invasion and Metastasis Research, Institute of Cancer Research, Capital Medical University, Beijing, China

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Yabin Hu Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Invasion and Metastasis Research, Institute of Cancer Research, Capital Medical University, Beijing, China

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Sai Wu Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Invasion and Metastasis Research, Institute of Cancer Research, Capital Medical University, Beijing, China

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Yang Geng Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Invasion and Metastasis Research, Institute of Cancer Research, Capital Medical University, Beijing, China

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Kai Lin Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Invasion and Metastasis Research, Institute of Cancer Research, Capital Medical University, Beijing, China

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Wei Wu Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Invasion and Metastasis Research, Institute of Cancer Research, Capital Medical University, Beijing, China
Institute of Brain Tumor, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, China

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cells ( Cao et al. 2010 ). Studies showed that sustained ERK1/2 phosphorylation by SFN induced apoptosis ( Li et al. 2014 , Peng et al. 2015 ), and transient ERK1/2 activation by SFN contributed to cancer progression in vitro ( Hsu et al. 2013

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-17-0483
Volume/Issue:
Volume 25: Issue 3
Free access
Philipp Y Maximov Department of Breast Medical Oncology, MD Anderson Cancer Centre, Houston, Texas, USA

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Balkees Abderrahman Department of Breast Medical Oncology, MD Anderson Cancer Centre, Houston, Texas, USA

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Ramona F Curpan Institute of Chemistry, Romanian Academy, Timisoara, Romania

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Yousef M Hawsawi Department of Genetics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia

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Ping Fan Department of Breast Medical Oncology, MD Anderson Cancer Centre, Houston, Texas, USA

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V Craig Jordan Department of Breast Medical Oncology, MD Anderson Cancer Centre, Houston, Texas, USA

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on acquired antihormone resistance. We discuss the similarities of the phenomenon of sex steroid-induced apoptosis in both types of cancers after acquisition of antihormone resistance and explore the possibility that this new knowledge will have

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-17-0416
Volume/Issue:
Volume 25: Issue 2
Open access
Ying-Cheng Chiang Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan

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Ming-Cheng Chang Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan

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Pao-Jen Chen Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan

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Meei-Maan Wu Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan

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Chang-Yao Hsieh Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan

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Wen-Fang Cheng Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan

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Chi-An Chen Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan

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-induced apoptosis of ovarian cancer cells. Materials and methods Patients and specimens The study protocol was reviewed and approved by the Institutional Review Board of the hospital. Advanced-staged, high-grade ovarian serous carcinoma patients undergoing debulking

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-12-0117
Volume/Issue:
Volume 20: Issue 2
Free access
S Krajewski The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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M Krajewska The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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B C Turner The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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C Pratt The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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B Howard The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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J M Zapata The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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V Frenkel The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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S Robertson The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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Y Ionov The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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H Yamamoto The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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M Perucho The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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S Takayama The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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J C Reed The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA.

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Dysregulation of normal programmed cell death mechanisms plays an important role in the pathogenesis and progression of breast cancer, as well as in responses of tumors to therapeutic intervention. Overexpression of anti-apoptotic members of the Bcl-2 family such as Bcl-2 and Bcl-X(L) has been implicated in cancer chemoresistance, whereas high levels of pro-apoptotic proteins such as Bax promote apoptosis and sensitize tumor cells to various anticancer therapies. Though the mechanisms by which Bcl-2 family proteins regulate apoptosis are diverse, ultimately they govern decision steps that determine whether certain caspase family cell death proteases remain quiescent or become active. To date, approximately 17 cellular homologs of Bcl-2 and at least 15 caspases have been identified in mammals. Other types of proteins may also modulate apoptotic responses through effects on apoptosis-regulatory proteins, such as BAG-1-a heat shock protein 70 kDa (Hsp70/Hsc70)-binding protein that can modulate stress responses and alter the functions of a variety of proteins involved in cell death and division. In this report, we summarize our attempts thus far to explore the expression of several Bcl-2 family proteins, caspase-3, and BAG-1 in primary breast cancer specimens and breast cancer cell lines. Moreover, we describe some of our preliminary observations concerning the prognostic significance of these apoptosis regulatory proteins in breast cancer patients, contrasting results derived from women with localized disease (with or without node involvement) and metastatic cancer.

Article Type:
Abstract
Volume/Issue:
Volume 6: Issue 1
Free access
Bok-Soon Lee Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology
Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology

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Hyun-Young Cha Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology
Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology

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Yoo Seob Shin Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology
Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology

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Yong-Sung Kim Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology
Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology

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Chul-Ho Kim Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology
Department of Otolaryngology, Center for Cell Death Regulating Biodrug, Department of Molecular Science and Technology

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-related apoptosis-inducing ligand (TRAIL) is an attractive anticancer agent because it can selectively kill tumor cells, but not normal cells ( Ashkenazi & Herbst 2008 ). There are two functional receptors for TRAIL, death receptor 4 (DR4) and 5 (DR5). Each contains

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-12-0405
Volume/Issue:
Volume 20: Issue 3
Free access
Carolin Maria Frisch
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Katrin Zimmermann
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Pia Zilleßen Institute of Pharmacology and Toxicology, Federal Institute for Drugs and Medical Devices (BfArM), University of Bonn, Sigmund-Freud-Straße 25, 53127 Bonn, Germany

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Alexander Pfeifer
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Kurt Racké
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Peter Mayer Institute of Pharmacology and Toxicology, Federal Institute for Drugs and Medical Devices (BfArM), University of Bonn, Sigmund-Freud-Straße 25, 53127 Bonn, Germany

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microplates (Greiner Bio-One, Frickenhausen, Germany) using Caspase-Glo 3/7 Assay (Promega) in accordance to the manufacturer's protocol. To study effects of cytokines which were upregulated in gene expression profiling (see Results) on apoptosis, cells were

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-14-0581
Volume/Issue:
Volume 22: Issue 4
Free access
Adwitiya Kar Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Yu Zhang Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Betelehem W Yacob Division of Medical Oncology, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Jordan Saeed Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Kenneth D Tompkins Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Stacey M Bagby Division of Medical Oncology, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Todd M Pitts Division of Medical Oncology, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Hilary Somerset Department of Pathology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Stephen Leong Division of Medical Oncology, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA

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Margaret E Wierman Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA
Research Service, Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, Colorado, USA

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Katja Kiseljak-Vassiliades Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA
Research Service, Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, Colorado, USA

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proliferation and triggered apoptosis in ACC cells, and decreased tumor growth in our newly established in vivo ACC PDX mouse model. Together these findings establish the importance of PBK as a pro-tumorigenic kinase in ACC and confirm its potential as a

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-19-0262
Volume/Issue:
Volume 26: Issue 10
Free access