Mechanisms of antineoplastic action of somatostatin analogs

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Published on Saturday, 15 June 2013

Abstract

Over the past decade, impressive antineoplastic activity of somatostatin analogs has been demonstrated in many tumor models.

More recent research has provided information regarding mechanisms underlying the antiproliferative and apoptosis-inducing actions of these compounds.

These include both 'direct' mechanisms that are sequellae of binding of somatostatin analogs to somatostatin receptors present on neoplastic cells and 'indirect' mechanisms related to effects of somatostatin analogs on the host.

The upregulation of intracellular tyrosine phosphatase activity triggered by binding of ligands to the type II somatostatin receptor has received considerable attention as a direct mechanism, not only because this activity is the converse of the tyrosine kinase activity associated with many peptide mitogen receptors, but also because the type II somatostatin receptor is frequently expressed by common human neoplasms, including breast cancer.

The potential importance of indirect mechanisms of action of somatostatin analogs, such as alterations in host insulin-like growth factor physiology, is emphasized by the in vivo antineoplastic activity of these compounds against somatostatin receptor-negative neoplasms.

Clinical efficacy and a favorable toxicity profile of somatostatin analogs in the treatment of relatively uncommon conditions such as acromegaly and neuroendocrine tumors have already been demonstrated.

Preclinical data now are sufficient to justify controlled clinical trials in breast, prostate, and pancreatic cancer. The development of monthly depot formulations will facilitate the clinical evaluation of somatostatin analogs for these and other indications.

 

 

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See also Somatostatin in oncology, the overlooked evidences.