Systemic Treatment of Gastroenteropancreatic Neuroendocrine Tumors (GEP-NETS): Cuirrent Approaches and Future Options

2014 ◽  
Vol 20 (2) ◽  
pp. 167-175 ◽  
Author(s):  
Jonathan Strosberg
Keyword(s):  
Neuroendocrine Tumors ◽  
Systemic Treatment ◽  
Gastroenteropancreatic Neuroendocrine Tumors

scholarly journals Local treatment for focal progression in metastatic neuroendocrine tumors

2019 ◽  
Vol 26 (4) ◽  
pp. 405-409 ◽  
Author(s):  
Taymeyah Al-Toubah ◽  
Stefano Partelli ◽  
Mauro Cives ◽  
Valentina Andreasi ◽  
Franco Silvestris ◽  
...  
Keyword(s):  
Median Time ◽  
Neuroendocrine Tumors ◽  
Systemic Treatment ◽  
Local Treatment ◽  
Arterial Embolization ◽  
External Beam Radiation ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Beam Radiation ◽  
Additional Intervention ◽  
Systemic Treatments

New systemic treatments have improved the therapeutic landscape for patients with metastatic gastroenteropancreatic neuroendocrine tumors (GEP-NETs). While drugs such as everolimus, sunitinib, temozolomide and 177Lutetium-dotatate are appropriate for patients with widespread disease progression, local treatment approaches may be more appropriate for patients with unifocal progression. Surgical resection, radiofrequency ablation (RFA), hepatic arterial embolization (HAE) or radiation, can control discrete sites of progression, allowing patients to continue their existing therapy and sparing them toxicities of a new systemic treatment. We identified 69 patients with metastatic GEP-NETs who underwent a local treatment for focal progression in the setting of widespread metastases. Twenty-six percent underwent resection, 27% RFA, 23% external beam radiation and 23% selective HAE. With a median follow-up of 25 months, 42 (61%) patients subsequently progressed to the point of requiring additional intervention (12 locoregional, 30 systemic) for disease control. Median time to new systemic treatment was 32 months (95% CI, 16.5–47.5 months). Median time to any additional intervention was 19 months (95% CI, 8.7–25.3 months). Control of local sites of progression enabled the majority of patients to remain on their existing systemic treatment and avoid potential toxicities associated with salvage systemic therapy.

Biology and Systemic Treatment of Advanced Gastroenteropancreatic Neuroendocrine Tumors

2018 ◽  
pp. 292-299 ◽  
Author(s):  
Nitya Raj ◽  
Nicola Fazio ◽  
Jonathan Strosberg
Keyword(s):  
Neuroendocrine Tumors ◽  
Systemic Treatment ◽  
Future Research ◽  
Neuroendocrine Neoplasms ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Treatment Approaches ◽  
Biologic Characterization ◽  
Scientific Advances

In recent years, there have been important scientific advances in the biologic characterization of neuroendocrine neoplasms and in their treatment. This review will describe these scientific advances, the evolving systemic treatment approaches, and important topics to be addressed in future research.

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

Advances in the Systemic Treatment of Neuroendocrine Tumors in the Era of Molecular Therapy

2013 ◽  
Vol 13 (3) ◽  
pp. 382-388 ◽  
Author(s):  
Roland Leung ◽  
Brian Lang ◽  
Hilda Wong ◽  
Joanne Chiu ◽  
Wan K. Yat ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Systemic Treatment ◽  
Molecular Therapy

scholarly journals SUNitinib and EVOfosfamide ( TH ‐302) in systemic treatment‐naïve patients with G1 / G2 metastatic pancreatic neuroendocrine tumors, the GETNE ‐1408 trial

2021 ◽  
Author(s):  
Enrique Grande ◽  
Cristina Rodriguez‐Antona ◽  
Carlos López ◽  
Teresa Alonso‐Gordoa ◽  
Marta Benavent ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Systemic Treatment ◽  
Pancreatic Neuroendocrine Tumors ◽  
Treatment Naïve

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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