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Correspondingly, GEP-NETs are classified as “functional” (F-NETs) or “nonfunctional” (NF-NETs) based on the presence or absence, respectively, of a specific clinical syndrome associated with hormone oversecretion.
Hormone secretion, however, does not uniformly result in a clinical syndrome, for example, as in the case of pancreatic polypeptide (PP) secretion.
PNETs are rare neoplasms, compared with carcinomas arising from pancreatic exocrine tissue.
They, like other neuroendocrine tumor types, display variable malignant potential, hormone-related syndromes (functionality), localization, and genetic background.
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This literature review briefly summarizes the epidemiology, pathophysiology, clinical management, and outcomes of patients with pancreatic neuroendocrine tumors (PNETs) and highlights recent advances in PNET research.
Thus, the cellular origin of PNETs is complex and remains to be elucidated.
The molecular basis of PNET pathogenesis is poorly characterized.
The average human islet consists of approximately 3,000 cells producing insulin (β cells, 54%), glucagon (α cells, 34%), somatostatin (δ cells, 10%), vasoactive intestinal polypeptide (VIP) (δcells), PP (PP cells), and substance P/serotonin (enterochromaffin cells).
Gastrin-producing G cells are present in fetal but not normal adult pancreatic islets [6, 39].
Surgery remains the primary therapeutic option for patients with PNETs.