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Alfred King-yin Lam School of Medicine, Griffith University, Gold Coast, Australia

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content of the chapters on this entity between the two editions of WHO book despite 13 years in between. It is worth noting that there is a proposed developmental relationship between anaplastic carcinoma and squamous cell carcinoma ( Lam & Saremi 2017

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-20-0045
Volume/Issue:
Volume 27: Issue 6
Free access
Soomin Ahn Department of Pathology, Ewha Womans University School of Medicine, Seoul, Korea

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Tae Hyuk Kim Division of Endocrinology and Metabolism, Department of Medicine, Thyroid Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Sun Wook Kim Division of Endocrinology and Metabolism, Department of Medicine, Thyroid Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Chang Seok Ki Department of Laboratory Medicine and Genetics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Hye Won Jang Department of Medical Education, Sungkyunkwan University School of Medicine, Seoul, Korea

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Jee Soo Kim Division of Breast and Endocrine Surgery, Department of Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Jung Han Kim Division of Breast and Endocrine Surgery, Department of Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Jun-Ho Choe Division of Breast and Endocrine Surgery, Department of Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Jung Hee Shin Department of Radiology and Center for Imaging Science, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Soo Yeon Hahn Department of Radiology and Center for Imaging Science, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Young Lyun Oh Department of Pathology and Translational genomics, Sungkyunkwan University School of Medicine, Seoul, Korea

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Jae Hoon Chung Division of Endocrinology and Metabolism, Department of Medicine, Thyroid Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

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Follicular carcinoma 61 (92.4%) 0 (0%) 5 (7.6%) 66 Poorly differentiated carcinoma 6 (100%) 0 (0%) 0 (0%) 6 Anaplastic carcinoma 7 (77.8%) 0 (0%) 2 (22.2%) 9 Total 380 (93.4%) 18 (4.4%) 9 (2.2%) 407

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-16-0421
Volume/Issue:
Volume 24: Issue 2
Free access
Yeon-Sook Choi Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea

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Hyemi Kwon Division of Endocrinology and Metabolism, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea

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Mi-Hyeon You Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea

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Tae Yong Kim Division of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea

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Won Bae Kim Division of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea

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Young Kee Shong Division of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea

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Min Ji Jeon Division of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea

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Won Gu Kim Division of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea

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Dabrafenib is a BRAF kinase inhibitor approved for treatment of BRAF-mutated anaplastic thyroid carcinoma (ATC) in combination with trametinib. Erlotinib is a tyrosine kinase inhibitor of EGF receptor (EGFR). We evaluated effects of dabrafenib and erlotinib combination treatment on ATC cells in vitro and in vivo. Cell proliferation, colony formation, apoptosis, and migration of ATC cells harboring a BRAF mutation (BHT101, 8505C, and SW1736) were evaluated after treatment with dabrafenib in combination with erlotinib or trametinib. The changes in activation of mitogen extracellular kinase (MEK) and extracellular signal-related kinase (ERK) signaling were also evaluated by Western blot analysis. Effects of these combinations were also evaluated using an in vivo xenograft model. First, we detected EGFR activation in dabrafenib-resistant SW1736 cells using a phospho-receptor tyrosine kinase array. A dabrafenib and erlotinib combination synergistically inhibited cell proliferation, colony formation, and migration, with an induction of apoptotic cell death in all three ATC cells, compared with dabrafenib or erlotinib alone. This synergistic effect was comparable with a dabrafenib and trametinib combination. The dabrafenib and erlotinib combination effectively inhibited phosphorylated (p)-MEK, p-ERK, and p-EGFR expressions compared with dabrafenib or erlotinib alone, while the dabrafenib and trametinib combination only inhibited p-MEK and p-ERK expressions. The dabrafenib with erlotinib or trametinib combinations also significantly suppressed tumor growth and induced apoptosis in a BHT101 xenograft model. The dabrafenib and erlotinib combination could be a potential novel treatment regimen to overcome drug resistance to dabrafenib alone in patients with BRAF-mutated ATC.

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-22-0022
Volume/Issue:
Volume 29: Issue 6
Restricted access
Devora Champa
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Marika A Russo
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Xiao-Hui Liao Department of Developmental and Molecular Biology, Departments of Medicine, Pediatrics and Committee on Genetics, Department of Pathology, Albert Einstein College of Medicine, Price Center for Genetic and Translational Medicine, 1301 Morris Park Avenue, Room 302, Bronx, New York 10461, USA

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Samuel Refetoff Department of Developmental and Molecular Biology, Departments of Medicine, Pediatrics and Committee on Genetics, Department of Pathology, Albert Einstein College of Medicine, Price Center for Genetic and Translational Medicine, 1301 Morris Park Avenue, Room 302, Bronx, New York 10461, USA
Department of Developmental and Molecular Biology, Departments of Medicine, Pediatrics and Committee on Genetics, Department of Pathology, Albert Einstein College of Medicine, Price Center for Genetic and Translational Medicine, 1301 Morris Park Avenue, Room 302, Bronx, New York 10461, USA

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Ronald A Ghossein Department of Developmental and Molecular Biology, Departments of Medicine, Pediatrics and Committee on Genetics, Department of Pathology, Albert Einstein College of Medicine, Price Center for Genetic and Translational Medicine, 1301 Morris Park Avenue, Room 302, Bronx, New York 10461, USA

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Antonio Di Cristofano
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) often tightly adhering to nearby anatomical structures. Figure 1 Kras G12D , p53 thyr−/− mice develop papillary thyroid cancer progressing to poorly differentiated and anaplastic carcinomas. (A) Cumulative tumor incidence for mice of the indicated

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-14-0268
Volume/Issue:
Volume 21: Issue 5
Free access
Alyaksandr V Nikitski Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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

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Linwah Yip Division of Endocrine Surgery, Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Esra Karslioglu-French Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Sally E Carty Division of Endocrine Surgery, Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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

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59 Male NA 6 p.R181H, 17.3% PTEN, p.R233*, 17.6% CNA PC,CT AC, anaplastic carcinoma; CNA, copy number alteration; CT,classic type; FA, follicular adenoma; FC, follicular carcinoma; FV, follicular variant; HCA, Hurthle cell

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-21-0095
Volume/Issue:
Volume 28: Issue 9
Restricted access
Esra Karslioglu French Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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

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Linwah Yip Division of Endocrine Surgery, Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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

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

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Sally E Carty Division of Endocrine Surgery, Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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EIFAX1 tumors were either low-grade cancers (60% EFVPTC) or NIFTP (20%), they also included anaplastic carcinoma which was found in 10% of nodules with more than two mutations. The latter tumors harbored multiple mutations, including TERT and TP53

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-22-0041
Volume/Issue:
Volume 29: Issue 8
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Dolly Thomas Department of Medicine, Department of Molecular, The Leon D. Black Family Stem Cell Institute, Mount Sinai School of Medicine, Box 1055, One Gustave L. Levy Place, New York, New York 10029, USA

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Susan Friedman Department of Medicine, Department of Molecular, The Leon D. Black Family Stem Cell Institute, Mount Sinai School of Medicine, Box 1055, One Gustave L. Levy Place, New York, New York 10029, USA

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Reigh-Yi Lin Department of Medicine, Department of Molecular, The Leon D. Black Family Stem Cell Institute, Mount Sinai School of Medicine, Box 1055, One Gustave L. Levy Place, New York, New York 10029, USA
Department of Medicine, Department of Molecular, The Leon D. Black Family Stem Cell Institute, Mount Sinai School of Medicine, Box 1055, One Gustave L. Levy Place, New York, New York 10029, USA
Department of Medicine, Department of Molecular, The Leon D. Black Family Stem Cell Institute, Mount Sinai School of Medicine, Box 1055, One Gustave L. Levy Place, New York, New York 10029, USA
Department of Medicine, Department of Molecular, The Leon D. Black Family Stem Cell Institute, Mount Sinai School of Medicine, Box 1055, One Gustave L. Levy Place, New York, New York 10029, USA

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follicular carcinomas of the thyroid have a very good prognosis. Medullary carcinoma forms in the C cells of the thyroid gland and has usually spread to other organs by the time of diagnosis. Anaplastic carcinoma is the most deadly form of thyroid cancer

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-07-0210
Volume/Issue:
Volume 15: Issue 1
Free access
Gahee Park Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of
Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Tae Hyuk Kim Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Hae-Ock Lee Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Jung Ah Lim Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of
Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Jae-Kyung Won Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Hye Sook Min Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Kyu Eun Lee Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Do Joon Park Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Young Joo Park Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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Woong-Yang Park Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of
Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of
Samsung Genome Institute, Internal Medicine, Surgery, Biomedical Sciences, Department of Internal Medicine, Department of Molecular Cell Biology, Samsung Medical Center, 50 Irwondong, Gangnamgu, Seoul 135-710, Korea Departments of

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and anaplastic carcinoma ( Godbert et al . 2014 , Kelly et al . 2014 ). Treatment with clinically available ALK inhibitors, such as crizotinib and TAE684, yielded in vitro antitumor efficacy ( Kelly et al . 2014 ) and produced clinical

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-14-0467
Volume/Issue:
Volume 22: Issue 1
Free access
Garcilaso Riesco-Eizaguirre Instituto de Investigaciones Biomédicas ‘Alberto Sols’,, Servicio de Endocrinología y Nutrición,, Consejo Superior de Investigaciones Científicas y Universidad Autónoma de Madrid (CSIC-UAM), 28029 Madrid, Spain
Instituto de Investigaciones Biomédicas ‘Alberto Sols’,, Servicio de Endocrinología y Nutrición,, Consejo Superior de Investigaciones Científicas y Universidad Autónoma de Madrid (CSIC-UAM), 28029 Madrid, Spain

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Pilar Santisteban Instituto de Investigaciones Biomédicas ‘Alberto Sols’,, Servicio de Endocrinología y Nutrición,, Consejo Superior de Investigaciones Científicas y Universidad Autónoma de Madrid (CSIC-UAM), 28029 Madrid, Spain

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5 to 10%. However, RAS mutations are more prevalent in poorly differentiated (55%) and anaplastic carcinoma (52%; Garcia-Rostan et al . 2003 ). Moreover, this group found a significant association between RAS mutations and poor survival, proposing

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-07-0085
Volume/Issue:
Volume 14: Issue 4
Free access
Haleh Vosgha Cancer Molecular Pathology, School of Medicine, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia

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Armin Ariana Cancer Molecular Pathology, School of Medicine, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia

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Robert Anthony Smith Cancer Molecular Pathology, School of Medicine, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia
Genomics Research Centre, Institute of Health and Biomedical Innovation, Faculty of Health, Queensland University of Technology, Brisbane, Queensland, Australia

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Alfred King-yin Lam Cancer Molecular Pathology, School of Medicine, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia

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( P  < 0.05) ( Fig. 2A and B ). This result confirmed the permanent ectopic expression of miR-205 in the anaplastic carcinoma cells (MB-1 and BHT-101). Figure 2 (A and B) Normalised relative expression of mir-205 by qRT-PCR to confirm

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-17-0497
Volume/Issue:
Volume 25: Issue 3
Free access