ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2007) 14 S17.2 
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Somatostatin receptors in neuroendocrine tumors

Kjell Oberg

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A unique feature of neuroendocrine tumors is that they express peptide hormone receptors. All five subtypes of somatostatin receptors are expressed in neuroendocrine tumors with dominance for receptor type 2 (SST2). Stimulation of SST2 can not only inhibit hormone release from the tumor, but also tumor cell growth. Both SST2 and 3 are involved in apoptosis of neuroendocrine tumor cells. SST’s in intratumoral blood vessels might implicate a role of anti-angiogenesis of somatostatin and somatostatin analogues. Midgut carcinoids express about 80% of the tumors SST2. The same is true for most endocrine pancreatic tumors, except for benign insulin producing tumors that has a lower expression (50%). Signaling through SST2 inhibit hormone release and causes antiproliferation, whereas stimulation of SST2 and 3 causes apoptosis. 111Indium-DTPA-octreotide (Octreoscan®) can be applied for localisation and staging of neuroendocrine tumors. Labelling of octreotide with either 177Lutetium or 90Yttrium is used for tumor targeted radioactive treatment (PRRT). The use of somatostatin analogues, Octreotide and Lanreotide, has been a real break-through in the management of functioning neuroendocrine tumors. Symptomatic and biochemical improvement has been noticed in 50-60% of the patients and tumor reduction in 5–10%. A new somatostatin analogue – SOM230 – has been applied in phase-2-trials. This analogue is binding with high affinity to receptor 1, 2, 3 and 5, but not 4. It has already demonstrated significant symptomatic effects in patients with functioning neuroendocrine tumors, resistant to octreotide treatment. In the future analysis of the expression pattern of different somatostatin receptors in neuroendocrine tumors will be important, particularly if new somatostatin analogues will be developed.

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