Filamin-A is involved in stabilisation, signal transduction, and angiogenesis regulation mediated by somatostatin receptor 2 in pancreatic neuroendocrine tumors

Author(s):  
Eleonora Vitali ◽  
Valeria Cambiaghi ◽  
Federica Loiarro ◽  
Alessandro Zerbi ◽  
Piergiuseppe Colombo ◽  
...  
Pancreas ◽  
2016 ◽  
Vol 45 (2) ◽  
pp. 187-192 ◽  
Author(s):  
Ki Byung Song ◽  
Song Cheol Kim ◽  
Ji Hun Kim ◽  
Dong-Wan Seo ◽  
Seung-Mo Hong ◽  
...  

Cancer ◽  
2013 ◽  
Vol 119 (23) ◽  
pp. 4094-4102 ◽  
Author(s):  
Kosuke Okuwaki ◽  
Mitsuhiro Kida ◽  
Tetuo Mikami ◽  
Hiroshi Yamauchi ◽  
Hiroshi Imaizumi ◽  
...  

Medicine ◽  
2015 ◽  
Vol 94 (40) ◽  
pp. e1281 ◽  
Author(s):  
Shreya Mehta ◽  
Philip R. de Reuver ◽  
Preetjote Gill ◽  
Juliana Andrici ◽  
Lisa D’Urso ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5117
Author(s):  
Chandra K. Maharjan ◽  
Po Hien Ear ◽  
Catherine G. Tran ◽  
James R. Howe ◽  
Chandrikha Chandrasekharan ◽  
...  

Pancreatic neuroendocrine tumors (pNETs) are unique, slow-growing malignancies whose molecular pathogenesis is incompletely understood. With rising incidence of pNETs over the last four decades, larger and more comprehensive ‘omic’ analyses of patient tumors have led to a clearer picture of the pNET genomic landscape and transcriptional profiles for both primary and metastatic lesions. In pNET patients with advanced disease, those insights have guided the use of targeted therapies that inhibit activated mTOR and receptor tyrosine kinase (RTK) pathways or stimulate somatostatin receptor signaling. Such treatments have significantly benefited patients, but intrinsic or acquired drug resistance in the tumors remains a major problem that leaves few to no effective treatment options for advanced cases. This demands a better understanding of essential molecular and biological events underlying pNET growth, metastasis, and drug resistance. This review examines the known molecular alterations associated with pNET pathogenesis, identifying which changes may be drivers of the disease and, as such, relevant therapeutic targets. We also highlight areas that warrant further investigation at the biological level and discuss available model systems for pNET research. The paucity of pNET models has hampered research efforts over the years, although recently developed cell line, animal, patient-derived xenograft, and patient-derived organoid models have significantly expanded the available platforms for pNET investigations. Advancements in pNET research and understanding are expected to guide improved patient treatments.


Oncotarget ◽  
2015 ◽  
Vol 7 (6) ◽  
pp. 6593-6608 ◽  
Author(s):  
Miguel Sampedro-Núñez ◽  
Raúl M. Luque ◽  
Ana M. Ramos-Levi ◽  
Manuel D. Gahete ◽  
Ana Serrano-Somavilla ◽  
...  

2015 ◽  
Vol 100 (6) ◽  
pp. 1089-1097 ◽  
Author(s):  
Ersin Gürkan Dumlu ◽  
Derya Karakoç ◽  
Arif Özdemir

In this article, we aimed to review the literature on the clinics and management of nonfunctional pancreatic neuroendocrine tumors (NPNET). Pancreatic neuroendocrine tumors (PNET) are rare tumors with a <1/100,000 incidence and constitute approximately 2 to 10% of all pancreatic tumors. Nonfunctional PNETs are difficult to detect at early stages since they have no symptoms. Except those detected accidentally during different diagnoses, the majority of PNETs are detected in the advanced stages, with symptoms related to tumor size or liver metastasis. We reviewed the studies published in the English medical literature through PubMed and summarized the clinical features and current approaches to the treatment and follow-up of the NPNET. The common imaging techniques used for the detection of tumor localization, size, locoregional, and metastatic involvement are contrasted computed tomography, magnetic resonance imaging, endoscopic ultrasonography, and somatostatin receptor scintigraphy. Surgical resection is the only curative treatment. However, in advanced locoregional disease and liver metastasis, interventive ablative therapies such as palliative reductive surgery, selective hepatic arterial embolization, radiofrequency ablation; and systemic therapies, such as peptide receptor radionuclide therapy, chemotherapy, somatostatin analogous therapy, interferon, VEGF inhibitor, and mTOR inhibitor may be used as symptom relieving or may improve progression-free survival and total survival. Current knowledge on NPNET shows that the treatment should be personalized considering the prognostic features and life expectancy of the patient.


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