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Johanna Sandgren, Teresita Diaz de Ståhl, Robin Andersson, Uwe Menzel, Arkadiusz Piotrowski, Helena Nord, Martin Bäckdahl, Nimrod B Kiss, Michael Brauckhoff, Jan Komorowski, Henning Dralle, Ola Hessman, Catharina Larsson, Göran Åkerström, Carl Bruder, Jan P Dumanski, and Gunnar Westin

metastases during 5 years of follow-up). In two of the cases with malignant paragangliomas, both the primary metastasis and the associated metastasis were studied. The samples were collected in tissue banks during a 20-year period from the Uppsala University

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Elizabeth Grubbs, Daniel Halperin, Steven G Waguespack, and Robert F Gagel

The multiple endocrine neoplasia (MEN) workshops had their beginnings at Queen’s University in Kingston, Ontario in June 1984. This initial meeting brought clinicians and scientists together to focus on mapping the gene for multiple endocrine neoplasia type 2 (MEN2). These efforts culminated in the identification of the RET protooncogene as the causative gene a decade later. Over the next 35 years there were a total of 16 international workshops focused on the several MEN syndromes. Importantly, these workshops were instrumental in efforts to define the molecular basis for multiple endocrine neoplasia type 1 (MEN1), MEN2, von Hippel-Lindau disease (VHL), Carney Complex, hereditary pheochromocytoma and hyperparathyroidism. In this same spirit some 150 scientists and clinicians met at MD Anderson Cancer Center, 27–29 March 2019, for the 16th International Workshop on Multiple Endocrine Neoplasia (MEN2019). Appropriate to its location in a cancer centre, the workshop focused on important issues in the causation and treatment of malignant aspects of the MEN syndromes: medullary thyroid carcinoma, pancreatic neuroendocrine tumours, malignant pheochromocytoma and parathyroid carcinoma. Workshops at the meeting focused on a better understanding of how the identified molecular defects in these genetic syndromes lead to transformation, how to apply targeted kinase inhibitors and immunotherapy to treat these tumours and important clinical management issues. This issue of Endocrine-Related Cancer describes these discussions and recommendations.

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L Fishbein, S Ben-Maimon, S Keefe, K Cengel, D A Pryma, A Loaiza-Bonilla, D L Fraker, K L Nathanson, and D L Cohen

-1907 ) 10.1210/jc.2013-1907 Niemeijer ND Alblas G van Hulsteijn LT Dekkers OM Corssmit EP 2014 Chemotherapy with cyclophosphamide, vincristine and dacarbazine for malignant paraganglioma and pheochromocytoma: systematic review and

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Maya B Lodish, Karen T Adams, Thanh T Huynh, Tamara Prodanov, Alex Ling, Clara Chen, Suzanne Shusterman, Camilo Jimenez, Maria Merino, Marybeth Hughes, Kendall W Cradic, Dragana Milosevic, Ravinder J Singh, Constantine A Stratakis, and Karel Pacak

tumour suppressors: a genetic and biochemical update . Nature Reviews. Cancer 5 857 – 866 . Havekes B Corssmit EP Jansen JC van der Mey AG Vriends AH Romijn JA 2007 Malignant paragangliomas associated with mutations in the succinate

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B Havekes, A A van der Klaauw, M M Weiss, J C Jansen, A G L van der Mey, A H J T Vriends, B A Bonsing, J A Romijn, and E P M Corssmit

frequently found. Recently, evaluation of the biochemical phenotype of SDHB-associated malignant paragangliomas revealed hypersecretion of norepinephrine, normetanephrine, and dopamine ( Timmers et al . 2007 b ). The reason for a different prevalence of

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Eamonn R Maher

tumour growth in nude mice assays. Malignant paragangliomas are known to be associated with germline SDHB mutations and although malignancy has yet to be reported in HIF2A -mutated tumours, the significance of HIF2A mutations for rate of tumour

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Bora E Baysal and Eamonn R Maher

than HNPGL or pheochromocytoma, and there is a significantly higher risk of malignant paraganglioma and poor prognosis (∼25% lifetime risk; Gimenez-Roqueplo et al . 2003 , Amar et al . 2007 , Ricketts et al . 2010 ). Despite the heterogeneity of

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Henri J L M Timmers, Anne-Paule Gimenez-Roqueplo, Massimo Mannelli, and Karel Pacak

Romijn JA 2007 Malignant paragangliomas associated with mutations in the succinate dehydrogenase D gene . Journal of Clinical Endocrinology and Metabolism 92 1245 – 1248 . Hull MT Roth LM Glover JL Walker PD 1982 Metastatic carotid

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Umasuthan Srirangalingam, Bernard Khoo, Lisa Walker, Fiona MacDonald, Robert H Skelly, Emad George, David Spooner, Linda B Johnston, John P Monson, Ashley B Grossman, W M Drake, Scott A Akker, Patrick J Pollard, Nick Plowman, Norbert Avril, Daniel M Berney, Jacky M Burrin, Rodney H Reznek, V K Ajith Kumar, Eamonn R Maher, and Shern L Chew

mutation carriers, malignant paragangliomas were evident in 31% of subjects, while no subjects have developed malignant disease in the VHL cohort to date. These data correlate with the larger tumour size noted in the SDHB mutation cohort compared with

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Hans K Ghayee, Bas Havekes, Eleonora P M Corssmit, Graeme Eisenhofer, Stephen R Hammes, Zahid Ahmad, Alexander Tessnow, Ivica Lazúrová, Karen T Adams, Antonio T Fojo, Karel Pacak, and Richard J Auchus

Jansen JC van der Mey AG Vriends AH Romijn JA 2007 Malignant paragangliomas associated with mutations in the succinate dehydrogenase D gene . Journal of Clinical Endocrinology and Metabolism 92 1245 – 1248 . van Houtum WH Corssmit EP