Related Experiment Video

Updated: Jun 4, 2026

A Practical Guide for the Production and PET/CT Imaging of 68Ga-DOTATATE for Neuroendocrine Tumors in Daily Clinical Practice
08:55

A Practical Guide for the Production and PET/CT Imaging of 68Ga-DOTATATE for Neuroendocrine Tumors in Daily Clinical Practice

Published on: April 17, 2019

Somatostatin analogs for the treatment of neuroendocrine tumors

Michael D Culler1, Kjell Oberg, Rudolf Arnold

  • 1Endocrinology Research, IPSEN, 27 Maple Street, Milford, MA 01757, USA. michael.culler@ipsen.com

Cancer Metastasis Reviews
|March 4, 2011
PubMed

Insights

Somatostatin analogs stabilize gastroenteropancreatic neuroendocrine tumors (GEP-NETs) and prolong survival. Novel therapies, including broader receptor binding analogs and radionuclide therapy, offer new treatment avenues for GEP-NETs.

Area of Science:

  • Endocrinology
  • Oncology
  • Pharmacology

Background:

  • Somatostatin regulates hormone release via specific receptors.
  • Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) express somatostatin receptors, indicating therapeutic potential.
  • Somatostatin analogs are established treatments for GEP-NETs, showing disease stabilization and survival benefits.

Purpose of the Study:

  • To review current data on somatostatin analog treatment for GEP-NETs.
  • To highlight findings from the PROMID study.
  • To discuss emerging therapies for GEP-NETs.

Main Methods:

  • Review of clinical trial data on somatostatin analogs in GEP-NETs.
  • Analysis of the PROMID study outcomes.
  • Survey of novel therapeutic strategies for GEP-NETs.

Main Results:

  • Somatostatin analogs demonstrate efficacy in stabilizing GEP-NETs and improving survival.
  • Recent findings indicate antiproliferative effects of somatostatin analogs.
  • Novel therapies under investigation include broader-acting analogs, chimeric molecules, combination therapies, and radionuclide therapy.

Conclusions:

  • Somatostatin analogs are a cornerstone in GEP-NET management.
  • Emerging therapies hold promise for enhanced treatment of GEP-NETs.
  • Further research into novel somatostatin-based therapies is warranted.

More Related Videos

Establishment and Characterization of Small Bowel Neuroendocrine Tumor Spheroids09:43

Establishment and Characterization of Small Bowel Neuroendocrine Tumor Spheroids

Published on: October 14, 2019

Related Concept Videos

Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...
Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
Phenothiazines, such as prochlorperazine...
Oral Hypoglycemic Agents: Sulfonylureas01:17

Oral Hypoglycemic Agents: Sulfonylureas

Sulfonylureas are oral hypoglycemic agents utilized in treating type 2 diabetes. They are characterized by their unique sulfonylurea chemical structure. The family of sulfonylureas is divided into generations. First-generation sulfonylureas, including tolbutamide (Orinase), chlorpropamide (Diabinese), and tolazamide (Tolinase), trigger insulin release from pancreatic β cells and enhance peripheral tissues' insulin sensitivity. The second-generation members, such as glipizide (Glucotrol),...
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...