Current treatment strategies for patients with advanced gastroenteropancreatic neuroendocrine tumors (GEP-NETs)

Uri, Inbal; Grozinsky‐Glasberg, Simona

doi:10.1186/s40842-018-0066-3

Cited by 55 publications

(48 citation statements)

References 68 publications

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“…The functional gastro-entero-pancreatic NETs (hormonally active GEP-NETs) include small bowel NETs (ileum and jejunum), which can produce serotonin, and maybe accompanied by a carcinoid syndrome. Functional pancreatic neuroendocrine tumors (f-pNETs) are able to produce gastrin, insulin, intestinal polypeptides and glucagon, and can lead to the occurrence of such clinical syndromes as ulcers, hypoglycemia, hyperglycemia and diarrhea [6]. Rare p-NETs like glucagonoma and VIPoma are associated with hypokalemia and watery diarrhea, but less frequently [3].…”

Section: Introductionmentioning

confidence: 99%

Assessment and State of Nutrition of Patients with Gastroenteropancreatic Neuroendocrine Neoplasms

et al. 2020

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Introduction: In recent decades, the number of gastro-entero-pancreatic neuroendocrine neoplasms (GEP-NENs) cases, associated with coexisting metabolic disorders, has been continuously increasing. Patients with progressing neoplastic disease are at a risk of malnutrition. To improve the quality of life of neuroendocrine neoplasms (NEN) patients, the therapeutic approach should be supported by a well-balanced diet. The aim of the study was to analyze the nutritional errors and deficits in a group of GEP-NET patients. Materials and methods: The study group included 26 GEP-NET patients; 13 men and 13 women. The mean age of women was 68.77 ± 8.0, and the mean age of men was 64.69 ± 8.1. Three interviews on consumption in the last 24 h were performed, in order to evaluate the quality and quantity of nutrition. The data was incorporated into a dietetics software, which allows one to calculate the number of over 58 micronutrients and macronutrients with the participation of 52 menus. Subsequently, the mean values were compared with the current nutritional standards. Results: An energy deficit was observed in the group of women—76.9%, and men—100%, as well as high fat consumption in 23.1% in both groups. The proportions of SFA/MUFA/PUFA were very negative, whereas the consumption of saccharose was too high. Vitamin D deficiency was observed in 100% of men and women. Moreover, both men and women experienced the deficiency of vitamin E, folates and niacin. The consumption of sodium and phosphorus was twice as high as recommended, and an insufficient supply of calcium was observed in 80% of women and 90% of men. The insufficient consumption of magnesium, iodine and potassium in a significant part of the studied group was observed. All participants consumed too much cholesterol and insufficient amounts of fiber. The healthy diet indicator (HDI) and diet quality index (DQI) scores were 3.1 ± 1.8 (HDI) and 3.7 ± 1.6 (DQI) for women, and 7.2 ± 2.6 (HDI) and 8.5 ± 2.4 (DQI) for men. Conclusions: When analyzing the nutrition of GEP-NET patients, we highlight that they do not have a proper diet, despite the fact that they changed the way they eat. Dietetics support and the development of official nutritional standards seem to be a necessary element in the therapy of GEP-NET patients.

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Section: Introductionmentioning

confidence: 99%

Assessment and State of Nutrition of Patients with Gastroenteropancreatic Neuroendocrine Neoplasms

et al. 2020

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“…On the other hand, a high tolerability is also related to low rates of drug interruption and discontinuation and consequently is likely to induce a better effectiveness. In this setting, whereas SSA are widely accepted as firstline treatment, because of their positive benefit/risk ratio, no data are available to establish the best choice as second-line treatment [22,23]. This is the first study with the purpose of trying to answer this unmet need, by analyzing and comparing the main therapeutic sequences in a large retrospective series of G1−G2 NET.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic sequences in patients with grade 1−2 neuroendocrine tumors (NET): an observational multicenter study from the ELIOS group

Faggiano

Maio²,

Mocerino

et al. 2019

Endocrine

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Your article is protected by copyright and all rights are held exclusively by Springer Science+Business Media, LLC, part of Springer Nature. This e-offprint is for personal use only and shall not be self-archived in electronic repositories. If you wish to selfarchive your article, please use the accepted manuscript version for posting on your own website. You may further deposit the accepted manuscript version in any repository, provided it is only made publicly available 12 months after official publication or later and provided acknowledgement is given to the original source of publication and a link is inserted to the published article on Springer's website. The link must be accompanied by the following text: "The final publication is available at link.springer.com".

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“…Finally, recent neuroendocrine tumor therapeutic efforts have included the investigation of inhibitors that target signaling in the Wnt/β-catenin, PI3K/AKT/mTOR, MET, and vascular endothelial factor pathways (8, 10, 11, 25, 41-59). PNETs and PECAs have been shown to differ in responsiveness to different therapies, depending on differences in types of drivers responsible for their biological behaviors (5,8,11,19,25,27,43,46,48,53,. In light of these findings, it is possible that EPB41L5 is a novel target for LG-PNET therapies.…”

Section: Figure 2 the Weak Epb41l5 Immunostaining Of A Primary Lg-pnmentioning

confidence: 99%

EPB41L5 is Associated With the Metastatic Potential of Low-grade Pancreatic Neuroendocrine Tumors

Saller

Seydafkan

Shahid

et al. 2019

Cancer Genomics Proteomics

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Background/Aim: Low-grade pancreatic neuroendocrine tumors (LG-PNETs) behave unpredictably. The aim of the study was to identify biomarkers that predict PNET metastasis to improve treatment selection. Patients and Methods: Five patients with primary non-metastatic LG-PNETs, six with primary LG-PNETs with synchronous or metachronous metastases (M-PNETs), and six metastatic to liver LG-PNETs (ML-PNETs) from the group of six M-PNET patients were selected. RNA data were normalized using iterative rank-order normalization. Student's t-test identified differentially-expressed genes in LG-PNETs versus M-PNETs. A 2-fold difference in expression was considered to be significant. Results were validated with an independent dataset of LG-PNETs and metastatic LG-PNETs. Results: Overall, 195 genes had a >2-fold change (in either direction). A total of 29 genes were differentially overexpressed in M-PNETs. Erythrocyte membrane protein band 4.1-like 5 (EPB41L5) had a 2.07-fold change increase in M-PNETs and the smallest p-value. EPB41L5 was not statistically different between M-PNETs and ML-PNETs. EPB41L5 differential expression between primary and metastatic LG-PNETs was confirmed by immunohistochemistry. Conclusion: These results support further investigation into whether EPB41L5 is a biomarker of PNETs with high risk for metastases. Pancreatic neuroendocrine tumors/carcinomas (PNETs/ PECAs) represent about 1-2% of all pancreatic tumors. Recently, however, it has been shown that PNETs have higher prevalence and malignant potential and result in considerable morbidity and mortality (1-4). This may be the result of increased physician awareness, increased use of advancements in imaging modalities, and the protracted clinical course of the disease (1). The oncogenic drivers responsible for the PNET metastatic phenotype have yet to be uncovered. As a result, these tumors are difficult to manage clinically because of their tendency to behave unpredictably (2). Indeed, even when considering low-grade PNETs (LG-PNETs), the presence of metastasis significantly affects patient survival and renders the tumors resistant to currently available therapies (5). Thus, the identification of a biomarker capable of identifying LG-PNETs at higher risk of metastasis may guide the clinical management of these tumors (3, 4). Published reports have shown that molecular alterations in PNETs include genomic alterations (GAs) in DNA damage repair genes MUTYH, CHEK2, and BRCA2 and inactivation of tumor suppressor genes and gene rearrangements that occur in MTAP, ARID2, SMARCA4, MLL3, CDKN2A, and SETD2 (6-12). Molecular analyses of PNETs have uncovered alterations in the pathways responsible for chromatin remodeling, DNA damage repair, activation of mammalian target of rapamycin (mTOR) signaling, and telomere maintenance. Moreover, gene expression profiling (GEP) of PNETs identified a subgroup of these tumors that are associated with hypoxia-inducible factor signaling (12). PNETs have also been reported to exhibit epithelial mesenchymal transition (EMT) b...

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Current treatment strategies for patients with advanced gastroenteropancreatic neuroendocrine tumors (GEP-NETs)

Cited by 55 publications

References 68 publications

Assessment and State of Nutrition of Patients with Gastroenteropancreatic Neuroendocrine Neoplasms

Assessment and State of Nutrition of Patients with Gastroenteropancreatic Neuroendocrine Neoplasms

Therapeutic sequences in patients with grade 1−2 neuroendocrine tumors (NET): an observational multicenter study from the ELIOS group

EPB41L5 is Associated With the Metastatic Potential of Low-grade Pancreatic Neuroendocrine Tumors

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