Pancreatic neuroendocrine neoplasms.
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Pancreatic neuroendocrine neoplasms. / Hörsch, D; Bert, T; Schrader, Jörg; Hommann, M; Kaemmerer, D; Petrovitch, A; Zaknun, J; Baum, R P.
in: Minerva Gastroenterol Dietol, Jahrgang 58, Nr. 4, 4, 2012, S. 401-426.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Pancreatic neuroendocrine neoplasms.
AU - Hörsch, D
AU - Bert, T
AU - Schrader, Jörg
AU - Hommann, M
AU - Kaemmerer, D
AU - Petrovitch, A
AU - Zaknun, J
AU - Baum, R P
PY - 2012
Y1 - 2012
N2 - Pancreatic neuroendocrine tumors originate from the diffuse neuroendocrine system in the pancreatic region. These tumors exhibit a rising incidence despite their rareness and due to their benign behavior a considerable prevalence. Pathogenesis of pancreatic neuroendocrine tumors is characterized by common pathways of hereditary and sporadic tumors. Pancreatic neuroendocrine tumors may secrete peptide hormones or biogenic amines in an autonomous fashion as functional active tumors. Pathological grading and staging by TNM systems has been established in recent years classifying well and moderately differentiated pancreatice neuroendocrine tumors and poorly differentiated neuroendocrine carcinomas. Chromogranin A and less so pancreatic polypeptide are suitable tumor markers for pancreatic neuroendocrine tumors. Expression of receptors for somatostatin is the basis of treatment of pancreatic neuroendocrine tumors with somatostatin analogues as antisecretive and antiproliferative agents. In addition, somatostatin scintigraphy or PET/CT allows comprehensive diagnosis of pancreatic neuroendocrine tumors, which should be supported by (endoscopic and contrast enhanced) ultrasound, CT and MRI. Therapy of pancreatic neuroendocrine tumors consists of somatostatin analogues, chemotherapy, targeted therapy and peptide receptor radionuclide therapy. Two molecular substances hav been registered for pancreatic neuroendocrine tumors recently, sunitinib (Sutent®) and everolimus (Afinitor®). Predominant tumor load in the liver may be treated by local ablative therapy or liver transplantation. These treatment options have been included in guidelines of several professional societies and weighted for sequential therapy of patients with pancreatic neuroendocrine tumors according to effects and side effects.
AB - Pancreatic neuroendocrine tumors originate from the diffuse neuroendocrine system in the pancreatic region. These tumors exhibit a rising incidence despite their rareness and due to their benign behavior a considerable prevalence. Pathogenesis of pancreatic neuroendocrine tumors is characterized by common pathways of hereditary and sporadic tumors. Pancreatic neuroendocrine tumors may secrete peptide hormones or biogenic amines in an autonomous fashion as functional active tumors. Pathological grading and staging by TNM systems has been established in recent years classifying well and moderately differentiated pancreatice neuroendocrine tumors and poorly differentiated neuroendocrine carcinomas. Chromogranin A and less so pancreatic polypeptide are suitable tumor markers for pancreatic neuroendocrine tumors. Expression of receptors for somatostatin is the basis of treatment of pancreatic neuroendocrine tumors with somatostatin analogues as antisecretive and antiproliferative agents. In addition, somatostatin scintigraphy or PET/CT allows comprehensive diagnosis of pancreatic neuroendocrine tumors, which should be supported by (endoscopic and contrast enhanced) ultrasound, CT and MRI. Therapy of pancreatic neuroendocrine tumors consists of somatostatin analogues, chemotherapy, targeted therapy and peptide receptor radionuclide therapy. Two molecular substances hav been registered for pancreatic neuroendocrine tumors recently, sunitinib (Sutent®) and everolimus (Afinitor®). Predominant tumor load in the liver may be treated by local ablative therapy or liver transplantation. These treatment options have been included in guidelines of several professional societies and weighted for sequential therapy of patients with pancreatic neuroendocrine tumors according to effects and side effects.
KW - Humans
KW - Treatment Outcome
KW - Prognosis
KW - Incidence
KW - Prevalence
KW - Magnetic Resonance Imaging
KW - Neoplasm Staging
KW - Endosonography
KW - Germany/epidemiology
KW - Antineoplastic Combined Chemotherapy Protocols/therapeutic use
KW - Neoplasm Grading
KW - Hepatectomy
KW - Biological Markers/blood
KW - Liver Transplantation
KW - Chromogranin A/blood
KW - Indoles/administration & dosage
KW - Neuroendocrine Tumors/blood/diagnosis/drug therapy/epidemiology
KW - Pancreatic Neoplasms/blood/diagnosis/drug therapy/epidemiology
KW - Positron-Emission Tomography and Computed Tomography
KW - Pyrroles/administration & dosage
KW - Sirolimus/administration & dosage/analogs & derivatives
KW - Somatostatin/analogs & derivatives
KW - Humans
KW - Treatment Outcome
KW - Prognosis
KW - Incidence
KW - Prevalence
KW - Magnetic Resonance Imaging
KW - Neoplasm Staging
KW - Endosonography
KW - Germany/epidemiology
KW - Antineoplastic Combined Chemotherapy Protocols/therapeutic use
KW - Neoplasm Grading
KW - Hepatectomy
KW - Biological Markers/blood
KW - Liver Transplantation
KW - Chromogranin A/blood
KW - Indoles/administration & dosage
KW - Neuroendocrine Tumors/blood/diagnosis/drug therapy/epidemiology
KW - Pancreatic Neoplasms/blood/diagnosis/drug therapy/epidemiology
KW - Positron-Emission Tomography and Computed Tomography
KW - Pyrroles/administration & dosage
KW - Sirolimus/administration & dosage/analogs & derivatives
KW - Somatostatin/analogs & derivatives
M3 - SCORING: Journal article
VL - 58
SP - 401
EP - 426
JO - Minerva Gastroenterol Dietol
JF - Minerva Gastroenterol Dietol
SN - 1121-421X
IS - 4
M1 - 4
ER -
