scholarly journals From biology to clinical experience: evolution in the knowledge of neuroendocrine tumours

2011 ◽  
Vol 2 (2) ◽  
pp. 79
Author(s):  
Emilio Bajetta ◽  
Giuseppe Procopio ◽  
Sara Pusceddu ◽  
Filippo Pietrantonio ◽  
Massimo Milione ◽  
...  
Keyword(s):  
Neuroendocrine Tumours ◽  
Clinical Course ◽  
Clinical Investigation ◽  
Target Therapy ◽  
Somatostatin Analogues ◽  
Good Activity ◽  
Multimodal Approach ◽  
Tumour Shrinkage ◽  
Biological Heterogeneity ◽  
Tumour Cell Growth

Neuroendocrine tumours (NETs) represent a group of neoplasias characterized by significant histopathological and biological heterogeneity. Diagnosis of neuroendocrine tumours relies upon histological examination augmented by newer techniques, such as pet-dotatoc scan. Surgery represents the only curative therapeutic approach. In advanced unresectable disease, medical treatment is the best choice. Somatostatin analogues allow adequate control of the carcinoid syndrome with a low effect on tumour cell growth. Chemotherapy has a good activity only in poor prognosis patients. According to the clinical course of the disease, a multimodal approach could be evaluated in selected cases. New target therapy including multikinase inhibitors, monoclonal antibody and m-tor inhibitors is now under clinical investigation for the treatment of advanced NETs. Preliminary results demonstrated a good activity in terms of disease control rate and tumour shrinkage.

scholarly journals Antitumour Effects of Somatostatin Analogues in the Treatment of Neuroendocrine Tumours

2012 ◽  
Vol 08 (03) ◽  
pp. 156
Author(s):  
Diogo Assed Bastos ◽  
Brenda Gumz ◽  
Frederico Costa ◽  
◽  
◽  
...  
Keyword(s):  
Neuroendocrine Tumours ◽  
Antitumour Activity ◽  
Somatostatin Receptors ◽  
Somatostatin Analogues ◽  
Antiangiogenic Activity ◽  
Tumour Shrinkage ◽  
Phosphotyrosine Phosphatases ◽  
Antitumour Effects

Neuroendocrine tumours (NETs) are rare and heterogeneous neoplasms that can present with functional syndromes due to the hypersecretion of peptides. Somatostatin analogues (SSAs) have been used since the 1980s for the treatment of neuroendocrine tumours, with the aim of controlling the symptoms of functioning tumours and improving patients’ quality of life. Data from preclinical studies offer evidence of both direct and indirect mechanisms by which SSAs can exert antitumour effects. The activation of somatostatin receptors by SSAs leads to the activation of phosphotyrosine phosphatases, which control downstream apoptotic and antiproliferation signalling pathways. Also, the suppression of secretion of several growth factors and inhibition of antiangiogenic activity by SSAs indirectly inhibits tumour cell proliferationin vitro. Previous uncontrolled studies had shown tumour shrinkage and disappearance in response to the SSA octreotide. Recent results from the randomised and placebo-controlled PROMID trial have demonstrated that octreotide has antitumour activity in patients with metastatic mid-gut NETs. This article examines recent data providing evidence of the antitumour activity of somatostatin analogues.

Antitumour Effects of Somatostatin Analogues in the Treatment of Neuroendocrine Tumours

2010 ◽  
Vol 8 (2) ◽  
pp. 94
Author(s):  
Diogo Assed Bastos ◽  
Brenda Gumz ◽  
Frederico Costa ◽  
◽  
◽  
...  
Keyword(s):  
Neuroendocrine Tumours ◽  
Antitumour Activity ◽  
Somatostatin Receptors ◽  
Somatostatin Analogues ◽  
Antiangiogenic Activity ◽  
Tumour Shrinkage ◽  
Phosphotyrosine Phosphatases ◽  
Antitumour Effects

Neuroendocrine tumours (NETs) are rare and heterogeneous neoplasms that can present with functional syndromes due to the hypersecretion of peptides. Somatostatin analogues (SSAs) have been used since the 1980s for the treatment of neuroendocrine tumours, with the aim of controlling the symptoms of functioning tumours and improving patients’ quality of life. Data from preclinical studies offer evidence of both direct and indirect mechanisms by which SSAs can exert antitumour effects. The activation of somatostatin receptors by SSAs leads to the activation of phosphotyrosine phosphatases, which control downstream apoptotic and antiproliferation signalling pathways. Also, the suppression of secretion of several growth factors and inhibition of antiangiogenic activity by SSAs indirectly inhibits tumour cell proliferationin vitro. Previous uncontrolled studies had shown tumour shrinkage and disappearance in response to the SSA octreotide. Recent results from the randomised and placebo-controlled PROMID trial have demonstrated that octreotide has antitumour activity in patients with metastatic mid-gut NETs. This article examines recent data providing evidence of the antitumour activity of somatostatin analogues.

[177Lu]Lu-DOTA-TATE Versus Standard of Care in Adult Patients With Gastro-Enteropancreatic Neuroendocrine Tumours (GEP-NETS): A Cost-Consequence Analysis From an Italian Hospital Perspective

2021 ◽  
Author(s):  
Francesca Spada ◽  
Davide Campana ◽  
Giuseppe Lamberti ◽  
Riccardo Laudicella ◽  
Renato Dellamano ◽  
...  
Keyword(s):  
Clinical Outcomes ◽  
Neuroendocrine Tumours ◽  
Treatment Options ◽  
Treatment Decision ◽  
Progression Free Survival ◽  
Standard Of Care ◽  
Somatostatin Analogues ◽  
Adult Patients ◽  
Hospital Perspective ◽  
Cost Consequence

Abstract Purpose To assess and compare clinical outcomes and costs, to the Italian healthcare system, of three therapeutic options approved in the management of adult patients with gastro-enteropancreatic neuroendocrine tumours (GEP-NETs). Methods We compared the efficacy, safety and costs of [177Lu]Lu-DOTA-TATE, everolimus (both originator and generic products) and sunitinib in patients with advanced GEP-NETs (NET G1 and G2) that had progressed following treatment with somatostatin analogues (SSAs). A cost-consequence model was developed and validated by a panel of clinical experts from three NET reference centres in Italy. The clinical outcomes included in the model were median progression-free survival and the incidence of grade 3 or 4 adverse events (AEs), as reported in pivotal clinical trials. The costs for acquisition and administration of each treatment, and of managing AEs, were calculated from the perspective of the Italian national health service. Treatment costs per progression-free month were calculated separately for patients with NETs of pancreatic (PanNETs; all three treatments) and gastrointestinal (GI-NETs; [177Lu]Lu-DOTA-TATE and everolimus only) origin. Results In patients with PanNETs, total costs per progression-free month were €2989 for [177Lu]Lu-DOTA-TATE, €4975 for originator everolimus, €3472 for generic everolimus, and €5337 for sunitinib. In patients with GI-NETs, total costs per progression-free month were €3189 for [177Lu]Lu-DOTA-TATE, €4990 for originator everolimus, and €3483 for generic everolimus. Conclusions [177Lu]Lu-DOTA-TATE was associated with lower costs per progression-free month versus relevant treatment options in patients with GI-NETs or PanNETs (NET G1–G2; progressed following SSA treatment), although acquisition and administration costs are higher. These findings provide further economic arguments in the overall context of treatment decision making.

Pancreatic endocrine disorders and multiple endocrine neoplasia

2020 ◽  
pp. 2449-2463
Author(s):  
B. Khoo ◽  
T.M. Tan ◽  
S.R. Bloom
Keyword(s):  
Kinase Inhibitors ◽  
Neuroendocrine Tumours ◽  
Mammalian Target Of Rapamycin ◽  
Peptide Receptor Radionuclide Therapy ◽  
Mtor Inhibitors ◽  
Somatostatin Analogues ◽  
Endocrine Disorders ◽  
Pancreatic Neuroendocrine Tumours ◽  
Islet Cell Tumours ◽  
Cancer Syndromes

Pancreatic neuroendocrine tumours (islet-cell tumours) are rare and usually sporadic, but they may be associated with complex familial endocrine cancer syndromes. Recognized types of pancreatic neuroendocrine tumours are those that are non-functioning (often advanced at diagnosis and presenting with mass effects due to the absence of symptoms attributable to hormone hypersecretion), insulinoma (the most frequent type), and others including gastrinoma, VIPoma, and glucagonoma. The following should be considered in addition to the symptomatic treatments: surgical resection—the only curative treatment, but not possible in many cases; tyrosine kinase inhibitors which inhibit specific kinases involved in tumour cell proliferation, growth, and angiogenesis; mammalian Target of Rapamycin (mTOR) inhibitors; peptide-receptor radionuclide therapy (radiolabelled somatostatin analogues).

Outcome of treating advanced neuroendocrine tumours with radiolabelled somatostatin analogues

2009 ◽  
Vol 11 (1) ◽  
pp. 48-53 ◽  
Author(s):  
María Angustias Muros ◽  
Mariela Varsavsky ◽  
Pablo Iglesias Rozas ◽  
Javier Valdivia ◽  
Juan Ramón Delgado ◽  
...  
Keyword(s):  
Neuroendocrine Tumours ◽  
Somatostatin Analogues

scholarly journals Neuroendocrine Carcinoma of the Uterine Cervix: A Clinicopathologic and Immunohistochemical Study with Focus on Novel Markers (Sst2–Sst5)

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1211
Author(s):  
Frediano Inzani ◽  
Angela Santoro ◽  
Giuseppe Angelico ◽  
Angela Feraco ◽  
Saveria Spadola ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Target Therapy ◽  
Somatostatin Receptors ◽  
Neuroendocrine Differentiation ◽  
Large Cell ◽  
Cell Types ◽  
Somatostatin Analogues ◽  
Small Cell ◽  
Neuroendocrine Neoplasms ◽  
Neuroendocrine Carcinomas

Background. Gynecological neuroendocrine neoplasms (NENs) are extremely rare, accounting for 1.2–2.4% of the NENs. The aim of this study was to test cervical NENs for novel markers of potential utility for differential diagnosis and target therapy. Methods. All cases of our center (n = 16) were retrieved and tested by immunohistochemistry (IHC) for 12 markers including markers of neuroendocrine differentiation (chromogranin A, synaptophysin, CD56), transcription factors (CDX2 and TTF1), proteins p40, p63, p16INK4a, and p53, somatostatin receptors subtypes (SST2-SST5) and the proliferation marker Ki67 (MIB1). Results. All cases were poorly differentiated neuroendocrine carcinomas (NECs), 10 small cell types (small cell–neuroendocrine carcinomas, SCNECs) and 6 large cell types (large cell–neuroendocrine carcinomas, LCNECs); in 3 cases a predominant associated adenocarcinoma component was observed. Neuroendocrine cancer cells expressed at least 2 of the 3 tested neuroendocrine markers; p16 was intensely expressed in 14 (87.5%) cases; SST5 in 11 (56.25%, score 2–3, in 9 cases); SST2 in 8 (50%, score 2–3 in 8), CDX2 in 8 (50%), TTF1 in 5 (31.25%), and p53 in 1 case (0.06%). P63 and p40 expressions were negative, with the exception of one case that showed moderate expression for p63. Conclusions. P40 is a more useful marker for the differential diagnosis compared to squamous cell carcinoma. Neither CDX2 nor TTF1 expression may help the differential diagnosis versus potential cervical metastasis. P16 expression may suggest a cervical origin of NEC; however, it must be always integrated by clinical and instrumental data. The expression of SST2 and SST5 could support a role for SSAs (Somatostatin Analogues) in the diagnosis and therapy of patients with cervical NECs.

scholarly journals The role of somatostatin analogues in the treatment of neuroendocrine tumours

2008 ◽  
Vol 286 (1-2) ◽  
pp. 238-250 ◽  
Author(s):  
Simona Grozinsky-Glasberg ◽  
Ashley B. Grossman ◽  
Márta Korbonits
Keyword(s):  
Neuroendocrine Tumours ◽  
Somatostatin Analogues
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