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

, pheochromocytoma; PGL, paraganglioma; PPGL, pheochromocytoma and paraganglioma. Pheochromocytoma in MEN2 and non-MEN2 familial forms PHEO are neuroendocrine tumors arising from adrenal medulla cells. Paragangliomas (PGL) originate form sympathetic

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Luis G Perez-Rivas, Andrea Oßwald, Thomas Knösel, Kristin Lucia, Christian Schaaf, Michael Hristov, Julia Fazel, Thomas Kirchner, Felix Beuschlein, Martin Reincke, and Marily Theodoropoulou

low-grade mediastinal paraganglioma, 1 choriocarcinoma and 2 were classified as carcinoma of unknown primary (CUP) tumor. Tissue was available only from liver metastasis in 2 cases. Overall, metastases were detected in 10 patients (3 with SCLC, 1 with

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Marta Vaquero, Anna Macià, Carlos Anerillas, Ana Velasco, Xavier Matias-Guiu, Joan Ribera, and Mario Encinas

Dear Editor, Pheochromocytomas (PCCs) are rare catecholamine-secreting tumors arising from the chromaffin cells in the adrenal medulla. Closely related paragangliomas share developmental origin but arise extra-adrenally in the paraganglia that

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E Patterson, R Webb, A Weisbrod, B Bian, M He, L Zhang, A K Holloway, R Krishna, N Nilubol, K Pacak, and E Kebebew

benign and malignant localized pheochromocytomas. Pheochromocytoma can be associated with autosomal hereditary cancer syndromes, such as multiple endocrine neoplasia type 2 (MEN2A and MEN2B), von Hippel–Lindau syndrome (VHL), paraganglioma syndrome type 1

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D Cecchin, F Lumachi, M C Marzola, G Opocher, C Scaroni, P Zucchetta, F Mantero, and F Bui

), negative predictive value (NPV) as (TN)/(TN + FN), and accuracy as (TN + TP) over all patients. Results Forty-eight (71.6%) patients thought to be affected by pheochromocytoma/paraganglioma underwent surgery followed by histological

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Yilun Deng, Shahida K Flores, ZiMing Cheng, Yuejuan Qin, Robin C Schwartz, Carl Malchoff, and Patricia L M Dahia

) ( Qin et al . 2014) . PHEOs and RCCs can arise as a result of inherited susceptibility, as in von Hippel Lindau disease and in PHEO-paraganglioma syndromes related to mutations in succinate dehydrogenase ( SDH ) subunit genes ( Maher 2011 , Dahia 2014

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H J L M Timmers, F M Brouwers, A R M M Hermus, F C G J Sweep, A A J Verhofstad, A L M Verbeek, K Pacak, and J W M Lenders

Year of diagnosis, features at presentation, and risk of recurrence in patients with pheochromocytoma or secreting paraganglioma . Journal of Clinical Endocrinology and Metabolism 90 2110 – 2116 . Benn DE Gimenez-Roqueplo AP Reilly JR

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Esther Korpershoek, Nanne K Kloosterhof, Angelique Ziel-van der Made, Hanneke Korsten, Lindsey Oudijk, Jan Trapman, Winand N M Dinjens, and Ronald R de Krijger

Hippel–Lindau (VHL) disease, neurofibromatosis type 1 and the PCC–paraganglioma (PGL) syndrome ( Neumann et al . 2002 ). The latter syndrome is characterized by both PCC and PGLs. PGLs are histologically similar to PCCs but are not always biochemically

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Dewi Astuti, Christopher J Ricketts, Rasheduzzaman Chowdhury, Michael A McDonough, Dean Gentle, Gail Kirby, Susanne Schlisio, Rajappa S Kenchappa, Bruce D Carter, William G Kaelin Jr, Peter J Ratcliffe, Christopher J Schofield, Farida Latif, and Eamonn R Maher

3 are frequent causes of inherited susceptibility to phaeochromocytoma or RCC. Thus, although Ladroue et al . (2008) reported a patient with recurrent paraganglioma and a germline PHD2 missense mutation (c.1121A→G, p.H374R, with loss of the

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Atanaska Elenkova, Rabhat Shabani, Elena Kinova, Vladimir Vasilev, Assen Goudev, and Sabina Zacharieva

histologically verified catecholamine secreting pheochromocytomas/paragangliomas (PPGL) and 24 subjects with essential hypertension (EH) matched for sex, age, BMI and glucose tolerance status. Fourteen patients had follow-up visits 18.4 ± 9.53 months after