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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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S M Fenkci, G Fidan Yaylali, Y Sermez, H Akdam, N Sabir, and S Kiraç

islet cell neoplasm with only six reported cases in the literature, and the pathophysiology remains unknown ( Anthony et al. 1995 ). Soga et al. (1998) collected a total of 407 cases from the international literature. They reported that the 10-year

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Dorota Dworakowska and Ashley B Grossman

frame shift Pancreatic islet cell neoplasm Lichenified hyperpigmented plagues suggesting a paraneoplastic process Merritt et al . (2006)  m Child 12 years TSC2 gene LOH in the tumour and the germ line mutation Q478X in exon 13 of the TSC2 gene on

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V Fendrich, C L Lopez, J Manoharan, K Maschuw, S Wichmann, A Baier, J P Holler, A Ramaswamy, D K Bartsch, and J Waldmann

2011b Hedgehog inhibition with the orally bioavailable Smo antagonist LDE225 represses tumor growth and prolongs survival in a transgenic mouse model of islet cell neoplasms . Annals of Surgery 254 818 – 823 . (discussion 823) ( doi:10.1097/SLA

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Sebastian Krug, Benjamin Kühnemuth, Heidi Griesmann, Albrecht Neesse, Leonie Mühlberg, Michael Boch, Juliane Kortenhaus, Volker Fendrich, Dominik Wiese, Bence Sipos, Juliane Friemel, Thomas M Gress, and Patrick Michl

transgenic mouse model of islet cell neoplasms . Annals of Surgery 254 818 – 823 . (discussion 823) ( doi:10.1097/SLA.0b013e318236bc0f ). Ghayouri M Boulware D Nasir A Strosberg J Kvols L Coppola D 2010 Activation of the serine

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

al . 1995 ). MEN1 MEN1 is an autosomal-dominant syndrome characterized by primary hyperparathyroidism, pancreatic islet cell neoplasms, and pituitary adenomas caused by inactivating mutations of the MEN1 locus coding for the suppressor protein menin

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Thorvardur R Halfdanarson, Joseph Rubin, Michael B Farnell, Clive S Grant, and Gloria M Petersen

). Korpássy (1939) found four cases (0.8%) of macroscopic islet cell adenomas in 500 autopsies in 1938. Twenty-four cases (0.3%) of ‘benign islet cell neoplasms’ were observed in a series of 9158 consecutive autopsies reported by Frantz (1959) . Warren et

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Marianne E Pavel and Christine Sers

S Wiese D Waldmann J Lauth M Rexin P L-Lopez C Schlitt HJ Bartsch DK Lang SA 2014 Inhibition of heat shock protein 90 with AUY922 represses tumor growth in a transgenic mouse model of islet cell neoplasms