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Frederic Castinetti, Jeffrey Moley, Lois Mulligan, and Steven G Waguespack

Introduction While the first clinical association between pheochromocytoma and medullary thyroid carcinoma (MTC) was described in 1961 by Sipple ( Sipple 1961 ), it was only 5 years later that the first description of oral mucosal neuromas in

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Angelica Malinoc, Maren Sullivan, Thorsten Wiech, Kurt Werner Schmid, Cordula Jilg, Joern Straeter, Serdar Deger, Michael M Hoffmann, Alexander Bosse, Gerd Rasp, Charis Eng, and Hartmut P H Neumann

germline mutations of the SDHB gene develop RCC in the setting of hereditary pheochromocytoma/PGL as well as Cowden syndrome, we sought to address the hypothesis that germline mutations in SDHC may also be associated with RCC by interrogating the

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Asterios Karagiannis, Dimitri P Mikhailidis, Vasilios G Athyros, and Faidon Harsoulis

sporadic pheochromocytomas or paragangliomas be screened for hereditary syndromes? Journal of Clinical Endocrinology and Metabolismm 91 2851 – 2858 . Johnson MD Smith PG Mills E Schanberg SM 1983 Paradoxical elevation of sympathetic activity

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Débora R Siqueira, Mírian Romitti, Andreia P da Rocha, Lucieli Ceolin, Camila Meotti, Aline Estivalet, Marcia K Puñales, and Ana Luiza Maia

. 2005 ). The MEN 2 syndrome includes three clinically distinct forms: MEN 2A, MEN 2B, and familial MTC (FMTC). In patients with FMTC, only the thyroid is affected. Patients with MEN 2A develop MTC, pheochromocytoma (PHEO), and/or primary

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Carole Guerin, Pauline Romanet, David Taieb, Thierry Brue, André Lacroix, Frederic Sebag, Anne Barlier, and Frederic Castinetti

development of pheochromocytoma (PHEO), and less frequently of hyperparathyroidism (HPTH). The aim of this review is first to detail the main characteristics and the management of MEN2 PHEO and then to define the main other etiologies of hereditary bilateral

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Francien H van Nederveen, Esther Korpershoek, Ronald J deLeeuw, Albert A Verhofstad, Jacques W Lenders, Winand N M Dinjens, Wan L Lam, and Ronald R de Krijger

Introduction Pheochromocytomas (PCC) are rare neuro-endocrine tumors arising from the adrenal medulla. Similar tumors arise from extra-adrenal chromaffin tissues, and are now referred to as sympathetic paragangliomas (PGLs; Baguet et al . 2004

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Esther Korpershoek, Claudia K Stobbe, Francien H van Nederveen, Ronald R de Krijger, and Winand N M Dinjens

Introduction Pheochromocytomas (PCCs) are rare catecholamine-producing neuroendocrine tumors arising from chromaffin cells of the adrenal medulla. Extra-adrenal sympathetic paragangliomas (sPGLs) were previously known as extra-adrenal PCC. sPGLs are

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Marta Kaczmarek-Ryś, Katarzyna Ziemnicka, Andrzej Pławski, Bartłomiej Budny, Michał Michalak, Szymon Hryhorowicz, Justyna Hoppe-Gołębiewska, Paweł Boruń, Monika Gołąb, Małgorzata Czetwertyńska, Maria Sromek, Marlena Szalata, Marek Ruchała, and Ryszard Słomski

gender, age at diagnosis, histopathological examination results with the evaluation of multifocality, the TNM classification and in patients with hereditary MTC also the presence of comorbid diseases: pheochromocytoma (PHEO) and primary

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Jenny Welander, Peter Söderkvist, and Oliver Gimm

.1–5.7%), of patients with neurofibromatosis type 1 develop pheochromocytomas ( Walther et al . 1999 ). Hereditary pheochromocytomas can also be observed in von Hippel–Lindau disease (10–26%) and multiple endocrine neoplasia type 2 (about 50%), as well as in

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Frederieke M Brouwers, Sven Gläsker, Amanda F Nave, Alexander O Vortmeyer, Irina Lubensky, Steven Huang, Mones S Abu-Asab, Graeme Eisenhofer, Robert J Weil, Deric M Park, W Marston Linehan, Karel Pacak, and Zhengping Zhuang

components of the machinery of catecholamine-producing cells. Recently, a common pathway has been suggested for the development of pheochromocytomas in hereditary syndromes ( Lee et al. 2005 a ). The authors propose that germline mutations in