Somatostatin analogues in the control of neuroendocrine tumours: efficacy and mechanisms

    1. Simona Grozinsky-Glasberg1,2,
    2. Ilan Shimon 2,
    3. Márta Korbonits1 and
    4. Ashley B Grossman1
    1. 1Barts and the London School of Medicine, Centre for Endocrinology, University of London, London EC1M 6BQ, UK2Institute of Endocrinology, Beilinson Hospital, Rabin Medical Center, and Sackler Faculty of Medicine, Tel Aviv 49100, Israel
    1. (Correspondence should be addressed to A B Grossman, Department of Endocrinology, St Bartholomew's Hospital, 5th Floor King George V Building, West Smithfield, London EC1A 7BE, UK; Email: a.b.grossman{at}


    Neuroendocrine tumours (NETs) represent a heterogeneous family of neoplasms, which may develop from different endocrine glands (such as the pituitary, the parathyroid or the neuroendocrine adrenal glands), endocrine islets (within the thyroid or pancreas) as well as from endocrine cells dispersed between exocrine cells throughout the digestive and respiratory tracts. The development of somatostatin analogues (SSA) as important diagnostic and treatment tools has revolutionised the clinical management of patients with NETs. However, although symptomatic relief and stabilisation of tumour growth for various periods of time are observed in many patients treated with SSA, tumour regression is rare. Possible mechanisms when this does occur include antagonism of local growth factor release and effects, probably including activation of tyrosine and serine–threonine phosphatases, and indirect effects via anti-angiogenesis. The development of new SSA, new drug combination therapies and chimaeric molecules should further improve the clinical management of these patients, as should a more complete understanding of their mode of action.

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