Journal
CLINICAL & TRANSLATIONAL ONCOLOGY
Volume 12, Issue 7, Pages 481-492Publisher
SPRINGER INTERNATIONAL PUBLISHING AG
DOI: 10.1007/s12094-010-0541-5
Keywords
Angiogenesis; Carcinoid; Everolimus; mTOR pathway; NETs; Neuroendocrine tumours; Pancreatic islet-cell carcinoma; Somatostatin analogues; Sunitinib; Treatment
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Funding
- MSD Oncology
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Neuroendocrine tumours (NET) of the digestive tract comprise a broad range of malignancies. The therapeutic approach to these tumours has not evolved as it did in other tumour types in the last two decades. The deeper knowledge of the underlying molecular biology behind the growth of neuroendocrine cells has brought much information to light. We now know that somatostatin analogues may not only be considered as symptomatic treatment but also as antitumour agents. Sunitinib, a tyrosine kinase (TK) inhibitor with antiangiogenic and antitumoural properties, has been shown to induce significant improvement in progression-free survival in a randomised trial conducted in well-differentiated pancreatic islet-cell NETs. The relevance of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway seems to be crucial in gastroenteropancreatic (GEP)-NETs. In fact, mTOR inhibitors have shown activity in uncontrolled trials, and large, randomised trial results will be available shortly. In this article, we summarise the most recent available data on medical therapy for GEPNETs.
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