Abstract
Gastroenteropancreatic neuroendocrine tumours (GEP NETs) are rare tumours that present many clinical features.They secrete peptides and neuroamines that cause distinct clinical syndromes, including carcinoid syndrome. However, many are clinically silent until late presentation with mass effects.In 2000 the WHO developed a new classification which gives a better description of the characteristics and biological behaviour of the tumour.Surgical resection is the treatment of first choice for a patient with a GEP NET. In metastatic disease multiple therapeutic approaches are possible. In these cases the goal is to improve quality of life and to extent survival.GEP NETs express somatostatin receptors (SSTRs), which are bound by somatostatin (SST) or its synthetic analogues, although the subtypes and number of SSTRs expressed is very variable.Somatostatin analogues are used frequently to control hormone-related symptoms while their anti-neoplastic activity, even if it has not been widely studied and the regarding data are discordant, seems to result prevalently in tumour stabilisation.A few patients who fail to respond or cease to respond to standard SST analogues treatment seem to have a response to higher doses of these drugs.The use of higher doses of somatostatin analogues or the development of new subtype selective agonists and chimaeric somatostatin analogues, or pan-somatostatin will probably improve the clinical management of these patients.This review provides an update on the use of somatostatin analogues in the management of GEP NETs and discusses novel clinical strategies based on SSTR 2 gene transfer therapy.
Highlights
Gastroenteropancreatic neuroendocrine tumours (GEP NETs) are an heterogeneous group of relatively rare tumours, whose yearly incidence is 1.2-3.0 cases/100,000 inhabitants [1].The database of the National Cancer Institute, Surveillance Epidemiology and End Results (SEER), mirroring the attention standards for US average patients, shows that the age-related incidence of small intestine and digestive tract carcinoids increased by 460% and 720% respectively, within a period of 30 years [2]
O’Toole et al in a multicentre study on 33 patients with the carcinoid syndrome comparing the treatment with lanreotide (30 mg i.m. every 10 days) versus octreotide (200 μg s.c. twice or thrice daily) founded no significant differences in controlling symptoms; 53.8% and 45.4%, respectively, of the patients treated with lanreotide referred disappearance or improvement in flushes and diarrhoea, while these symptoms were observed in 68% and 50%, respectively, of patients on octreotide
Vezzosi et al recently assessed that octreotide was effective in the control of hypoglycaemia in more than 50% of the insulinoma patients
Summary
Gastroenteropancreatic neuroendocrine tumours (GEP NETs) are an heterogeneous group of relatively rare tumours, whose yearly incidence is 1.2-3.0 cases/100,000 inhabitants [1]. Fykse et al treated five patients with hypergastrinaemia and gastric carcinoids for a period of 1 year with monthly injections of octreotide-LAR with a significant reduction in tumour load, ECL cell density and normalisation of circulating chromogranin A levels, indicating a possible direct antiproliferative effect of the treatment [83] These results suggest that the somatostatin analogues could have an important antiproliferative effect. Tomassetti et al have reported that after one-year therapy, the tumour completely disappeared in three patients suffering from gastric carcinoid, two of whom were treated with lanreotide 30 mg i.m. every 10 days [92] Cirillo in his retrospective study on 165 patients with digestive NETs confirmed that somatostatin analogs can have a role in the treatment of digestive neuroendocrine tumors with low grades of malignancy, a low cellular proliferation index and a high specific receptorial density in vivo, showing a SD ranging from 60 to 66%. Primary tumour growth and angiogenesis were highly decreased and associated with a reduction in microvessel density, inhibition of intratumoural production of VEGF and up-regulation of antiangiogenic SSTR 3 receptor expression in peripheral tumour vessels [32,113,114]
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