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Huy Gia Vuong Department of Pathology, University of Yamanashi, Chuo, Yamanashi, Japan

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Toru Odate Department of Pathology, University of Yamanashi, Chuo, Yamanashi, Japan

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Hanh T T Ngo Department of Pathology, University of Medicine and Pharmacy, Ho Chi Minh City, Vietnam

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Thong Quang Pham Department of Pathology, Cho Ray Hospital, Ho Chi Minh City, Vietnam

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Thao T K Tran Faculty of Medicine, University of Medicine and Pharmacy, Ho Chi Minh City, Vietnam

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Kunio Mochizuki Department of Pathology, University of Yamanashi, Chuo, Yamanashi, Japan

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Tadao Nakazawa Department of Pathology, University of Yamanashi, Chuo, Yamanashi, Japan

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Ryohei Katoh Department of Pathology, University of Yamanashi, Chuo, Yamanashi, Japan

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Tetsuo Kondo Department of Pathology, University of Yamanashi, Chuo, Yamanashi, Japan

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of MEN2 syndrome and about 50% of sporadic MTCs ( DeLellis et al . 2004 , Elisei et al . 2008 ). The second most common mutation in MTCs is RAS mutation, prevalence of which ranges from 10 to 60% of RET- negative MTCs in various studies, with

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-18-0056
Volume/Issue:
Volume 25: Issue 6
Free access
David L Vesely Division of Endocrinology, Diabetes and Metabolism, Departments of Medicine, Molecular Pharmacology and Physiology, James A. Haley VA Medical Center-151, University of South Florida Cardiac Hormone Center, and University of South Florida Morsani School of Medicine, 13000 Bruce B. Downs Boulevard, Tampa, Florida 33612, USA

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converts GTP to cyclic GMP ( Waldman et al . 1984 ). Cyclic GMP has a strong anticancer effect of decreasing human pancreatic cancer cell volume in vivo by 95% ( Vesely et al . 2004 ). Cyclic GMP inhibits the activation of kinases in the Ras–MEK 1/2–ERK

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-13-0054
Volume/Issue:
Volume 20: Issue 3
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Margarida M Moura Unidade de Investigação em Patobiologia Molecular (UIPM), Serviço de Endocrinologia, Clínica Universitária de Endocrinologia, Instituto Português de Oncologia de Lisboa Francisco Gentil E.P.E., Rua Prof. Lima Basto, 1099-023 Lisboa, Portugal

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Branca M Cavaco Unidade de Investigação em Patobiologia Molecular (UIPM), Serviço de Endocrinologia, Clínica Universitária de Endocrinologia, Instituto Português de Oncologia de Lisboa Francisco Gentil E.P.E., Rua Prof. Lima Basto, 1099-023 Lisboa, Portugal

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Valeriano Leite Unidade de Investigação em Patobiologia Molecular (UIPM), Serviço de Endocrinologia, Clínica Universitária de Endocrinologia, Instituto Português de Oncologia de Lisboa Francisco Gentil E.P.E., Rua Prof. Lima Basto, 1099-023 Lisboa, Portugal
Unidade de Investigação em Patobiologia Molecular (UIPM), Serviço de Endocrinologia, Clínica Universitária de Endocrinologia, Instituto Português de Oncologia de Lisboa Francisco Gentil E.P.E., Rua Prof. Lima Basto, 1099-023 Lisboa, Portugal
Unidade de Investigação em Patobiologia Molecular (UIPM), Serviço de Endocrinologia, Clínica Universitária de Endocrinologia, Instituto Português de Oncologia de Lisboa Francisco Gentil E.P.E., Rua Prof. Lima Basto, 1099-023 Lisboa, Portugal

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RAS in human cancer Introduction RAS research begins in 1964 with an observation by Jennifer Harvey (1964) that a murine leukemia virus, obtained from a leukemic rat, induced sarcomas in new-born rodents. Three additional

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-15-0070
Volume/Issue:
Volume 22: Issue 5
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Miguel A Zaballos Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Madrid, Spain
Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain

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Adrián Acuña-Ruiz Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Madrid, Spain
Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain

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Marta Morante Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain
Instituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Consejo Superior de Investigaciones Científicas (CSIC), Universidad de Cantabria, Santander, Spain

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Piero Crespo Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain
Instituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Consejo Superior de Investigaciones Científicas (CSIC), Universidad de Cantabria, Santander, Spain

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Pilar Santisteban Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Madrid, Spain
Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain

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of effective treatments for advanced thyroid carcinomas. Thyroid cancer is essentially an ERK-driven carcinoma. BRAF (rapidly accelerated fibrosarcoma type-B) mutations are found in up to 60% of PTC, followed by mutations in the different RAS

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-19-0098
Volume/Issue:
Volume 26: Issue 6
Free access
Vassiliki Kotoula
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Elias Sozopoulos Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece

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Helen Litsiou Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece

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Galinos Fanourakis Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece

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Triantafyllia Koletsa
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Gerassimos Voutsinas Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece

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Sophia Tseleni-Balafouta Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece

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Constantine S Mitsiades Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece
Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece

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Axel Wellmann Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece

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Nicholas Mitsiades Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece
Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece
Department of Pathology, Department of Pathology, Laboratory of Environmental Mutagenesis and Carcinogenesis, Department of Medical Oncology, Department of Medicine, Institute of Pathology, Memorial Sloan-Kettering Cancer Center, School of Medicine, Aristotle University of Thessaloniki, University Campus, Thessaloniki 54006, Greece

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identify new targets for tailored therapies. The Raf kinase family comprises A-Raf, B-Raf, and C-Raf (also called Raf-1) that play central roles in the conserved Ras/Raf/MEK/ERK pathway. The latter acts to relay signals from cell surface receptors, such as

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-08-0101
Volume/Issue:
Volume 16: Issue 2
Free access
Fabio L Forti Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo, Brazil

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Hugo A Armelin Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo, Brazil

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dependent on RhoA-GTP and involves drastic cellular morphological alterations. Amplification and overexpression of the K-ras oncogene is a major oncogenic lesion underlying the malignant state of the Y1 adrenocortical cell line ( Schwab et al . 1983

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-07-0154
Volume/Issue:
Volume 14: Issue 4
Free access
Branca M Cavaco Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and
Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and

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Pedro F Batista Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and

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Carmo Martins Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and

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Ana Banito Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and

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Francisco do Rosário Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and

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Edward Limbert Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and

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Luís G Sobrinho Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and
Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and

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Valeriano Leite Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and
Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and
Serviço de Endocrinologia, Faculdade de Ciências Médicas da Universidade Nova de Lisboa, Faculdade de Medicina de Lisboa, Centro de Investigação de Patobiologia Molecular (CIPM) and

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majority of sporadic PTC, and a significant proportion of the FTA/FTC, harbours activating mutations in genes from the RAS/RAF pathway ( Kimura et al . 2003 , Vasko et al . 2003 ), no oncogenic germline mutations have been detected in the K -, N

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-07-0214
Volume/Issue:
Volume 15: Issue 1
Free access
Chiara Laezza Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy
Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Anna Maria Malfitano Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Maria Chiara Proto Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Iolanda Esposito Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Patrizia Gazzerro Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Pietro Formisano Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Simona Pisanti Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Antonietta Santoro Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Maria Gabriella Caruso Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Maurizio Bifulco Institute of Endocrinology e Experimental Oncology, Department of Biology and Cellular, Department of Pharmaceutical Sciences, National Institute of Digestive Diseases, CNR, Via Pansini 5, 80131 Naples, Italy

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Ras family proteins ( Laezza et al . 2006 a , b ). The rate-limiting enzyme for the synthesis of MVA is HMG-CoA reductase, a critical regulator of cell proliferation in normal as well as in tumor cells ( Bifulco et al . 1995 ). At the transcriptional

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-10-0009
Volume/Issue:
Volume 17: Issue 2
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Janos Geli
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Nimrod Kiss
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Fredrik Lanner
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Theodoros Foukakis
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Natalia Natalishvili
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Olle Larsson
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Per Kogner
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Anders Höög
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Geoffrey J Clark
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Tomas J Ekström
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Martin Bäckdahl
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Filip Farnebo
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Catharina Larsson
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Introduction The Ras family consists of small GTP-binding proteins with an established role in basic cellular functions related to growth, differentiation and apoptosis. Upon activation, Ras molecules can contribute to tumorigenesis

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-06-0031
Volume/Issue:
Volume 14: Issue 1
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Marie-Claude Hofmann Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Muthusamy Kunnimalaiyaan Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Jennifer R Wang Department of Head and Neck Surgery, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Naifa L Busaidy Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Steven I Sherman Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Stephen Y Lai Department of Head and Neck Surgery, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Mark Zafereo Department of Head and Neck Surgery, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Maria E Cabanillas Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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signaling molecules such as RAS and protein kinases functioning in signaling cascades ( Fig. 1 ). Phosphorylation through protein kinases regulates key cellular processes that include gene expression, proliferation, differentiation, motility, membrane

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-22-0129
Volume/Issue:
Volume 29: Issue 11
Free access