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Department of Endocrinology, Amsterdam University Medical Centers, VU University Medical Center, Amsterdam, The Netherlands
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, have not been studied for insulinoma. Several immunohistochemical markers may be of use in separating indolent from aggressive insulinomas. Diffuse cytoplasmic insulin expression is seen in 90–100% of indolent insulinomas ( Roth et al. 1992
ENETS Center of Excellence, University Hospital Tübingen, Tübingen, Germany
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potential. Glucagon serum level may serve as tumor marker for monitoring patients during surveillance. Some anecdotal GCHN cases with liver metastasis are known in the scientific community, but none of these cases has been published so far ( Yu 2018
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Donatello Bone Clinic, Villa Donatello Hospital, Sesto Fiorentino, Italy
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-fold higher than wild-type littermates, expressing embryonic markers ( Vuguin & Charron 2011 ). The presence of pancreatic tumors in GCHN is usually associated with abdominal pain and discomfort but not with the glucagonoma syndrome, since glucagon
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the ducts. These nesidioblastotic features can be seen in the adult pancreas and are even more pronounced in the neonate pancreas. They usually need immunostaining for pancreatic hormones or neuroendocrine markers to be clearly identified ( Fig. 1F
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), second-generation SSAs (pasireotide), molecular-targeted therapies (MTT) (mTOR inhibitors (mTORi; everolimus)), or tyrosine kinase inhibitors (TKI; sunitinib) have been used. A further systemic targeted therapy is peptide receptor radionuclide therapy