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Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Munich, Germany
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Dear Editor, We greatly appreciate the comments by Gergely Huszty and Peter Igaz, published in this issue of Endocrine-Related Cancer article ID e230220 , on our review ‘Risk of complications after core needle biopsy in pheochromocytoma/paraganglioma
Human Molecular Genetics, de Duve Institute, Université catholique de Louvain, Brussels, Belgium
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Cardiology Department, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium
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Dear Editor, Pheochromocytomas and paragangliomas (PPGL) are rare neuroendocrine tumors arising from the adrenal medulla and extra-adrenal paraganglia, respectively. Forty percent are explained by germline mutations in known susceptibility
Department of Medical Genetics, Department of Clinical Genetics, University of Cambridge, Cambridge, UK and
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oxygen-dependent prolyl hydroxylases are inactive, pVHL-dependent degradation of HIFα subunits is compromised and HIF1 and HIF2 are stabilised and activate downstream transcriptional pathways. A notable feature of pheochromocytoma and paraganglioma is the
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stromal tumor (GIST; at the time gastric ‘leiomyosarcoma’), paraganglioma, and pulmonary chondroma. While it is traditional to use the term GIST in describing the gastric lesions in Carney triad, they are probably better described as ‘gastric stromal
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Assistance Publique – Hôpitaux de Marseille (AP-HM), Hôpital de la Conception, Centre de Référence des Maladies Rares Hypophysaires HYPO, Marseille, France
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cells or tumor, the middle syllables chromo refer to the former usage of a special chromate-containing stain and pheo refers to the classic brown appearance after exposure to chromate staining ( Bausch et al . 2017 b ). In contrast, paraganglioma
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third epibranchial placode (nodose placode) ( Baker 2005 ). Vagal paragangliomas Tumor origin and molecular genetics Vagus nerve paraganglia belong to the family of parasympathetic paraganglia. Members act as chemoreceptors and are involved
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Introduction SDH-deficient gastrointestinal stromal tumors (GISTs) are rare but sometimes lethal tumors that can occur in patients with paraganglioma (PGL) syndromes. These tumors do not harbor the KIT or PDGFRA mutations typical of
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Lady Davis Institute, Jewish General Hospital and Research Institute, McGill University Health Centre, Montreal, Quebec, Canada
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treatments ( Terzolo et al . 2014 ). Whether or not DICER1 mutations are present in adrenocortical cancer remains to be seen, but they could present a much-needed therapeutic target for this disease. DICER1 mutations in paragangliomas Similar to
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. 2001 ) have recently been described in familial paragangliomas and pheochromocytomas. Several reasons make these genes candidate tumor suppressors for MTC: (1) allelic loss of the short and long arm of chromosome 1, the localization of SDHB and SDHC
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Introduction Pheochromocytomas and paragangliomas (PPGL) are neuroendocrine tumors derived from chromaffin cells of the adrenal medulla or extraparaganglionic tissue ( Tischler 2008 ). Measurements of plasma-free normetanephrine and