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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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. During thyroid cancer evolution, the process from differentiated to undifferentiated thyroid carcinoma undergoes molecular and genetic alterations ( Kitahara & Sosa 2016 ). Multiple specific genetic mutations have been identified, such as BRAF, RAS, TERT

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-18-0193
Volume/Issue:
Volume 26: Issue 1
Free access
Steven E Justiniano Division of Endocrinology, Diabetes, and Metabolism, The Ohio State University, Columbus, OH, USA

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Joseph P McElroy Center for Biostatistics and Department of Bioinformatics, The Ohio State University, Columbus, OH, USA

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Lianbo Yu Center for Biostatistics and Department of Bioinformatics, The Ohio State University, Columbus, OH, USA

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Ayse Selen Yilmaz Center for Biostatistics and Department of Bioinformatics, The Ohio State University, Columbus, OH, USA

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Kevin R Coombes Center for Biostatistics and Department of Bioinformatics, The Ohio State University, Columbus, OH, USA

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Leigha Senter Division of Human Genetics, The Ohio State University, Columbus, OH, USA

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Rebecca Nagy Division of Human Genetics, The Ohio State University, Columbus, OH, USA
Guardant Health, Inc, Redwood City, California, USA

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Paul Wakely Jr Department of Pathology, The Ohio State University, Columbus, OH, USA

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Stefano Volinia Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Italy

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Michelle Vinco Department of Pathology, University of Michigan, Ann Arbor, Michigan, USA

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Thomas J Giordano Department of Pathology, University of Michigan, Ann Arbor, Michigan, USA
Comprehensive Cancer Center, University of Michigan, Ann Arbor, Michigan, USA

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Carlo M Croce Department of Molecular Virology, Immunology, and Genetics, The Ohio State University Wexner Medical Center and Arthur G. James Comprehensive Cancer Center, Columbus, Ohio, USA

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Motoyasu Saji Division of Endocrinology, Diabetes, and Metabolism, The Ohio State University, Columbus, OH, USA

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Matthew D Ringel Division of Endocrinology, Diabetes, and Metabolism, The Ohio State University, Columbus, OH, USA
Department of Molecular Virology, Immunology, and Genetics, The Ohio State University Wexner Medical Center and Arthur G. James Comprehensive Cancer Center, Columbus, Ohio, USA

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. ( doi:10.1091/mbc.E15-05-0259 ) Sohn SY Park WY Shin HT Bae JS Ki CS Oh YL Kim SW Chung JH 2016 Highly concordant key genetic alterations in primary tumors and matched distant metastases in differentiated thyroid

Article Type:
Letter
DOI:
https://doi.org/10.1530/ERC-16-0351
Volume/Issue:
Volume 23: Issue 10
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
Jessica L Geiger Division of Hematology/Oncology, Department of Internal Medicine, University of Pittsburgh Cancer Institute, Division of Anatomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Pittsburgh Medical Center, Division of Molecular Genomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, 5150 Centre Avenue, 5th Floor, Pittsburgh, Pennsylvania, 15232, USA

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Simion I Chiosea Division of Hematology/Oncology, Department of Internal Medicine, University of Pittsburgh Cancer Institute, Division of Anatomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Pittsburgh Medical Center, Division of Molecular Genomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, 5150 Centre Avenue, 5th Floor, Pittsburgh, Pennsylvania, 15232, USA

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Sue M Challinor Division of Hematology/Oncology, Department of Internal Medicine, University of Pittsburgh Cancer Institute, Division of Anatomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Pittsburgh Medical Center, Division of Molecular Genomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, 5150 Centre Avenue, 5th Floor, Pittsburgh, Pennsylvania, 15232, USA

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Marina N Nikiforova Division of Hematology/Oncology, Department of Internal Medicine, University of Pittsburgh Cancer Institute, Division of Anatomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Pittsburgh Medical Center, Division of Molecular Genomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, 5150 Centre Avenue, 5th Floor, Pittsburgh, Pennsylvania, 15232, USA

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Julie E Bauman Division of Hematology/Oncology, Department of Internal Medicine, University of Pittsburgh Cancer Institute, Division of Anatomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Pittsburgh Medical Center, Division of Molecular Genomic Pathology, Department of Pathology, University of Pittsburgh Medical Center, 5150 Centre Avenue, 5th Floor, Pittsburgh, Pennsylvania, 15232, USA

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( Debelenko et al . 1997 ). This pattern of bi-allelic loss of function is consistent with a tumor suppressor, as is noted in MEN1 neoplasms, and authors proposed that MEN1 genetic alterations are the first defined pathogenic abnormality for sporadic lung

Article Type:
Editorial
DOI:
https://doi.org/10.1530/ERC-15-0307
Volume/Issue:
Volume 22: Issue 5
Free access
Leland W K Chung Medicine and Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA

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-targeting both the tumor and the host stromal microenvironment. Together with Chinghai Kao, Tom Gardner, Arthur Ko, Hong Rhee, and Ken Koeneman, we developed the concept of osteomimicry, investigated the genetic alterations of cancer cells when subjected to 3D co

Article Type:
Other
DOI:
https://doi.org/10.1530/ERC-13-0433
Volume/Issue:
Volume 20: Issue 6
Free access
Federica Panebianco Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Alyaksandr V Nikitski Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Marina N Nikiforova Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Cihan Kaya Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Linwah Yip Division of Endocrine Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Vincenzo Condello Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Abigail I Wald Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Yuri E Nikiforov Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Simion I Chiosea Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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type. One PDTC showed an additional genetic alteration, TERT C250T mutation (Case #6, Table 2 ), whereas all other tumors had an ALK fusion as the only driver mutation identified. Figure 2 Histopathologic features of poorly differentiated

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-19-0325
Volume/Issue:
Volume 26: Issue 11
Restricted access
Willem E Corver Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands

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Hans Morreau Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands

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observed in Hürthle cell adenomas (HCA) ( Corver et al . 2017 ). The occurrence of genetic alterations in Hürthle cell hyperplasia and HCA was also studied by Nikiforova et al . in their evaluation of the ThyroSeq v3 genomic classifier for preoperative

Article Type:
Letter
DOI:
https://doi.org/10.1530/ERC-18-0481
Volume/Issue:
Volume 26: Issue 3
Free access
Deeqa Ahmed Department of Cancer Prevention, Centre for Cancer Biomedicine, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, PO Box 4953 Nydalen, NO-0424 Oslo, Norway
Department of Cancer Prevention, Centre for Cancer Biomedicine, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, PO Box 4953 Nydalen, NO-0424 Oslo, Norway

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Ragnhild A Lothe Department of Cancer Prevention, Centre for Cancer Biomedicine, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, PO Box 4953 Nydalen, NO-0424 Oslo, Norway
Department of Cancer Prevention, Centre for Cancer Biomedicine, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, PO Box 4953 Nydalen, NO-0424 Oslo, Norway

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Edgar Rivedal Department of Cancer Prevention, Centre for Cancer Biomedicine, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, PO Box 4953 Nydalen, NO-0424 Oslo, Norway
Department of Cancer Prevention, Centre for Cancer Biomedicine, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, PO Box 4953 Nydalen, NO-0424 Oslo, Norway

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Guro E Lind Department of Cancer Prevention, Centre for Cancer Biomedicine, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, PO Box 4953 Nydalen, NO-0424 Oslo, Norway
Department of Cancer Prevention, Centre for Cancer Biomedicine, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, PO Box 4953 Nydalen, NO-0424 Oslo, Norway

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of colorectal cancer, encodes a regulator of cytokinesis . Oncogene 30 3967 – 3978 . doi:10.1038/onc.2011.109 . Meling GI Lothe RA Børresen AL Hauge S Graue C Clausen OP Rognum TO 1991 Genetic alterations within the

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-11-0204
Volume/Issue:
Volume 18: Issue 6
Free access
William D Foulkes Departments of Human Genetics, Medicine and Oncology, McGill University, Montreal, Québec, Canada

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Jérôme Bertherat Department of Endocrinology, Cochin Hospital, Paris Descartes University, Paris, France

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Charis Eng Genomic Medicine Institute, Lerner Research Institute and Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio, USA
Department of Genetics and Genome Sciences and Germline High Risk Focus Group, Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA

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their US and Canadian collaborators ( Goudie et al. 2018 ) this complex and evolving field is efficiently summarized. It clearly shows that almost all endocrine glands have been found to possess genetic alterations in at least one tumor susceptibility

Article Type:
Editorial
DOI:
https://doi.org/10.1530/ERC-18-0283
Volume/Issue:
Volume 25: Issue 8
Free access
Berna C Özdemir Department of Oncology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
International Cancer Prevention Institute, Epalinges, Switzerland

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George Sflomos ISREC – Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland

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Cathrin Brisken International Cancer Prevention Institute, Epalinges, Switzerland
ISREC – Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland

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which genetic alterations are induced might influence whether mammary tumors are ER positive. For example, Lin and colleagues reported that deletion of P53 in prepubertal/pubertal mice, but not in adult mice, leads to the development of ER+ tumors

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-18-0063
Volume/Issue:
Volume 25: Issue 5
Free access