scholarly journals The recent European approval of lutetium (177Lu) oxodotreotide increases treatment options for gastroenteropancreatic neuroendocrine tumors

2018 ◽  
Vol 5 (2) ◽  
pp. IJE09 ◽  
Author(s):  
Martyn Caplin
Keyword(s):  
Neuroendocrine Tumors ◽  
Treatment Options ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
European Approval

scholarly journals Emerging Treatment Options for Gastroenteropancreatic Neuroendocrine Tumors

2020 ◽  
Vol 9 (11) ◽  
pp. 3655
Author(s):  
Mauro Cives ◽  
Eleonora Pelle’ ◽  
Jonathan Strosberg
Keyword(s):  
Clinical Trials ◽  
Growth Factor ◽  
Neuroendocrine Tumors ◽  
Treatment Options ◽  
Somatostatin Receptor ◽  
Growth Factor Receptor ◽  
Small Samples ◽  
Neuroendocrine Neoplasms ◽  
Two Phase ◽  
Gastroenteropancreatic Neuroendocrine Tumors

Treatment options for neuroendocrine tumors (NETs) and carcinomas (NECs) are expanding. Early-phase studies have shown preliminary evidence of the antitumor activity of alpha-emitting peptide receptor radionuclide therapy (PRRT), and novel radiopeptides incorporating somatostatin receptor antagonists (rather than agonists) have been developed. Several tyrosine kinase inhibitors (TKIs) with antiangiogenic potential have been evaluated in patients with NETs, including lenvatinib, axitinib, cabozantinib and pazopanib. Recently, two phase 3 clinical trials have demonstrated the efficacy and safety of surufatinib, an inhibitor of vascular endothelial growth factor receptor (VEGFR)-1, -2, -3, fibroblast growth factor receptor (FGFR)-1 and colony stimulating factor-1 receptor (CSF-1R), in patients with pancreatic and extra-pancreatic NETs. Multiple clinical trials of combination immunotherapy have been recently completed, but interpretation of the results is hampered by small samples sizes and discordant outcomes. This review summarizes recent data on emerging treatments for neuroendocrine neoplasms.

scholarly journals Current treatment options for gastroenteropancreatic neuroendocrine tumors with a focus on the role of lanreotide

2017 ◽  
Vol 2 ◽  
pp. 115-122 ◽  
Author(s):  
Beata Kos-Kudła ◽  
Jarosław Ćwikła ◽  
Marek Ruchała ◽  
Alicja Hubalewska-Dydejczyk ◽  
Barbara Jarzab ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Treatment Options ◽  
Current Treatment ◽  
Gastroenteropancreatic Neuroendocrine Tumors

scholarly journals GEP–NETs UPDATE: Radionuclide therapy in neuroendocrine tumors

2015 ◽  
Vol 172 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
Wouter A van der Zwan ◽  
Lisa Bodei ◽  
Jan Mueller-Brand ◽  
Wouter W de Herder ◽  
Larry K Kvols ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Targeted Therapies ◽  
Radionuclide Therapy ◽  
Randomized Clinical Trials ◽  
Treatment Options ◽  
Objective Response ◽  
Somatostatin Analogs ◽  
Peptide Receptor Radionuclide Therapy ◽  
Treatment Modalities ◽  
Gastroenteropancreatic Neuroendocrine Tumors

Peptide receptor radionuclide therapy (PRRT) is a promising new treatment modality for inoperable or metastasized gastroenteropancreatic neuroendocrine tumors (GEPNETs) patients. Most studies report objective response rates in 15–35% of patients. Also, outcome in terms of progression free survival (PFS) and overall survival compares very favorably with that for somatostatin analogs, chemotherapy, or new, ‘targeted’ therapies. They also compare favorably to PFS data for liver-directed therapies. Two decades after the introduction of PRRT, there is a growing need for randomized controlled trials comparing PRRT to ‘standard’ treatment, that is treatment with agents that have proven benefit when tested in randomized trials. Combining PRRT with liver-directed therapies or with targeted therapies could improve treatment results. The question to be answered, however, is whether a combination of therapies performed within a limited time-span from one another results in a better PFS than a strategy in which other therapies are reserved until after (renewed) tumor progression. Randomized clinical trials comparing PRRT with other treatment modalities should be undertaken to determine the best treatment options and treatment sequelae for patients with GEPNETs.

scholarly journals PI3K/mTOR Dual Inhibitor PF-04691502 Is a Schedule-Dependent Radiosensitizer for Gastroenteropancreatic Neuroendocrine Tumors

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1261
Author(s):  
Zeta Chow ◽  
Jeremy Johnson ◽  
Aman Chauhan ◽  
Tadahide Izumi ◽  
Michael Cavnar ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Treatment Options ◽  
Peptide Receptor Radionuclide Therapy ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Simultaneous Treatment ◽  
Mtor Inhibition ◽  
Dual Inhibitor ◽  
Dual Inhibitors ◽  
Dual Inhibition ◽  
New Treatment

Patients with advanced-stage gastroenteropancreatic neuroendocrine tumors (GEP-NETs) have a poor overall prognosis despite chemotherapy and radiotherapy (e.g., peptide receptor radionuclide therapy (PRRT)). Better treatment options are needed to improve disease regression and patient survival. The purpose of this study was to examine a new treatment strategy by combining PI3K/mTOR dual inhibition and radiotherapy. First, we assessed the efficacy of two PI3K/mTOR dual inhibitors, PF-04691502 and PKI-402, to inhibit pAkt and increase apoptosis in NET cell lines (BON and QGP-1) and patient-derived tumor spheroids as single agents or combined with radiotherapy (XRT). Treatment with PF-04691502 decreased pAkt (Ser473) expression for up to 72 h compared with the control; in contrast, decreased pAkt expression was noted for less than 24 h with PKI-402. Simultaneous treatment with PF-04691502 and XRT did not induce apoptosis in NET cells; however, the addition of PF-04691502 48 h after XRT significantly increased apoptosis compared to PF-04691502 or XRT treatment alone. Our results demonstrate that schedule-dependent administration of a PI3K/mTOR inhibitor, combined with XRT, can enhance cytotoxicity by promoting the radiosensitivity of NET cells. Moreover, our findings suggest that radiotherapy, in combination with timed PI3K/mTOR inhibition, may be a promising therapeutic regimen for patients with GEP-NET.

Is proliferative index (Ki-67) useful to stratify patients (pts) with G2 gastroenteropancreatic neuroendocrine tumors (GEP-NETs)? Clinicopathologic correlation.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 255-255
Author(s):  
Martin Angel ◽  
Juan O Connor ◽  
Veronica Pesce ◽  
Guillermo Ariel Mendez ◽  
Claudia Bestani ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Roc Curve ◽  
Target Therapy ◽  
Treatment Options ◽  
Rank Test ◽  
Roc Curve Analysis ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Ki 67 ◽  
Kaplan Meier

255 Background: Grade 2 (G2) Neuroendocrine tumors (NETs), of the digestive tract is a heterogeneous group of tumors. Several treatment options including chemotherapy and target therapy are available, but there is a lack of prospective trials assessing the role of pronostic factors in this population. Aim(s): to analyze prognostic factors and clinical characteristics in a population of patients with G2 GEP-NETs. To determine the role of ki 67 in the stratification of G2 population. Methods: Study population was obtained from our prospective database (Argentum Group). Survival was estimated using the Kaplan-Meier method and compared between Ki-67 quartiles using the log-rank test. Value of Ki-67 to discriminate mortality was assesed with a ROC curve analysis Results: 144 pts were evaluated. Mean age 54.9, 46.7% male. 102 (70.8%) with metastatic disease, mainly hepatic in 97 pts. (67.4%). 67.9 % underwent surgery. 34% received chemotherapy, and 10.9% target therapy. Median Ki-67 value was 6 (IQR 4-10), ROC curve=0.62 (95% CI 0.53 a 0.72 p=0.021. cut-off: 6.5 (sensitivity 62.2%, specificity 57.7%). Median survival was 97, 67, 51 and 27 months according stratification by quartile (p.001), 45 events (31.7%). Conclusions: Our results suggest that in the heterogenous G2 GEP-NETs there are significant differences in survival. This study was underpowered to detect differences between Ki-67 quartiles, we detected that chemotherapy was mostly used in the higher quartiles.

Gastroenteropancreatic neuroendocrine tumors: descriptive study in a reference Spanish hospital

2013 ◽  
Author(s):  
Zayas Beatriz Leon de ◽  
Olmo Garcia Maria Isabel del ◽  
Agustin Ramos Prol ◽  
Antonia Perez Lazaro ◽  
Susana Tenes Rodrigo ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Descriptive Study ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Spanish Hospital

Evaluation of neurofibromatosis type 1 and gastroenteropancreatic neuroendocrine tumors.

2018 ◽  
Author(s):  
Juan Carlos Percovich ◽  
Jose Atencia ◽  
Rogelio Garcia ◽  
Marcel Sambo ◽  
Montserrat Blanco ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Neurofibromatosis Type 1 ◽  
Neurofibromatosis Type ◽  
Gastroenteropancreatic Neuroendocrine Tumors

scholarly journals The state of PRRT and its sequencing amongst current therapeutic options for gastroenteropancreatic neuroendocrine tumors

2021 ◽  
Author(s):  
Lauren M Raymond ◽  
Tetiana Korzun ◽  
Adel Kardosh ◽  
Kenneth J. Kolbeck ◽  
Rodney Pommier ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Standard Dose ◽  
Peptide Receptor Radionuclide Therapy ◽  
Somatostatin Analogues ◽  
Tumor Burden ◽  
Treatment Modalities ◽  
Its Sequencing ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Reduce Tumor Burden ◽  
Spectrum Of Patients

Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are the most common form of neuroendocrine neoplasia, but there is no current consensus for the sequencing of approved therapies, particularly with respect to peptide receptor radionuclide therapy (PRRT). This comprehensive review evaluates the data supporting approved therapies for GEP-NETs and recommendations for therapeutic sequencing with a focus on how PRRT currently fits within sequencing algorithms. The current recommendations for PRRT sequencing restrict its use to metastatic, inoperable, progressive midgut NETs, however, this may change with emerging data to suggest PRRT might be beneficial as neoadjuvant therapy for inoperable tumors, is more tolerable than other treatment modalities following first-line standard dose somatostatin analogues, and can be used as salvage therapy after disease relapse following prior successful cycles of PRRT. PRRT has also been shown to reduce tumor burden, improve quality of life, and prolong the time to disease progression in a broad spectrum of patients with GEP-NETs. As the various potential benefits of PRRT in GEP-NET therapy continues to expand, it is necessary to review and critically evaluate our treatment algorithms for GEP-NETs.

scholarly journals Assessment of γ-H2AX and 53BP1 Foci in Peripheral Blood Lymphocytes to Predict Subclinical Hematotoxicity and Response in Somatostatin Receptor-Targeted Radionuclide Therapy for Advanced Gastroenteropancreatic Neuroendocrine Tumors

Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1516
Author(s):  
Thorsten Derlin ◽  
Natalia Bogdanova ◽  
Fiona Ohlendorf ◽  
Dhanya Ramachandran ◽  
Rudolf A. Werner ◽  
...  
Keyword(s):  
Treatment Response ◽  
Neuroendocrine Tumors ◽  
Peripheral Blood ◽  
Somatostatin Receptor ◽  
Therapy Response ◽  
Strand Break ◽  
Peripheral Blood Lymphocytes ◽  
Radioligand Therapy ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Blood Lymphocytes

Background: We aimed to characterize γ-H2AX and 53BP1 foci formation in patients receiving somatostatin receptor-targeted radioligand therapy, and explored its role for predicting treatment-related hematotoxicity, and treatment response. Methods: A prospective analysis of double-strand break (DSB) markers was performed in 21 patients with advanced gastroenteropancreatic neuroendocrine tumors. γ-H2AX and 53BP1 foci formation were evaluated in peripheral blood lymphocytes (PBLs) at baseline, +1 h and +24 h after administration of 7.4 GBq (177Lu)Lu-DOTA-TATE. Hematotoxicity was evaluated using standard hematology. Therapy response was assessed using (68Ga)Ga-DOTA-TATE PET/CT before enrollment and after 2 cycles of PRRT according to the volumetric modification of RECIST 1.1. Results: DSB marker kinetics were heterogeneous among patients. Subclinical hematotoxicity was associated with γ-H2AX and 53BP1 foci formation (e.g., change in platelet count vs change in γ-H2AX+ cells between baseline and +1 h (r = −0.6080; p = 0.0045). Patients showing early development of new metastases had less γ-H2AX (p = 0.0125) and less 53BP1 foci per cell at +1 h (p = 0.0289), and demonstrated a distinct kinetic pattern with an absence of DSB marker decrease at +24 h (γ-H2AX: p = 0.0025; 53BP1: p = 0.0008). Conclusions: Assessment of γ-H2AX and 53BP1 foci formation in PBLs of patients receiving radioligand therapy may hold promise for predicting subclinical hematotoxicity and early treatment response.

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