Current Treatments of Neuroendocrine Tumors Role of Biotherapy and Chemotherapy

2003 ◽  
Vol 89 (2) ◽  
pp. 111-116 ◽  
Author(s):  
Silvia Della Torre ◽  
Giuseppe Procopio ◽  
Alberto Fusi ◽  
Laura Catena ◽  
Leonardo Ferrari ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Standard Treatment ◽  
Somatostatin Analogues ◽  
Interferon Α ◽  
Hormone Release ◽  
Tumor Patients ◽  
Medical Treatments ◽  
Oncological Centers ◽  
Poorly Differentiated

Neuroendocrine tumors are rare neoplasms originating from cells belonging to a diffuse or confined neuroendocrine system and characterized by a significant histopatologic and biologic heterogeneity. Timely diagnosis is delayed because they are often clinically silent for their low differentiation grade and the absence of any symptom due to abnormal hormone release. For these reasons, many neuroendocrine tumor patients are not treated medically for metastatic or inoperable disease. Medical treatments include biotherapy, with interferon-α and somatostatin analogues, and chemotherapy. Somastostatin analogues are widely used in patients with symptoms and with carcinoids of low differentiation grade. Interferon-α is used alone or in combination with somatostatin analogues. Chemotherapy is active in patients with poorly differentiated neuroendocrine tumors. The therapeutic regimen commonly used is the combination of cisplatinum and etoposide. In conclusion, no standard treatment for NET has yet been identified, and the response criteria suggested by ITMO remain a reference point. The clinical aspect of the disease and biologic features suggest the identification of neuroendocrine tumors patients suitable for the appropriate therapies. On these bases, it is recommended that diagnosis and treatment of neuroendocrine tumors be carried out at specialized oncological centers involved in clinical trials.

scholarly journals Small Bowel and Colorectal Carcinoids

2018 ◽  
Vol 31 (05) ◽  
pp. 301-308 ◽  
Author(s):  
Raphael Byrne ◽  
Rodney Pommier
Keyword(s):  
Small Bowel ◽  
Neuroendocrine Tumors ◽  
Cytoreductive Surgery ◽  
Mammalian Target Of Rapamycin ◽  
Arterial Embolization ◽  
Angiogenesis Inhibitors ◽  
Somatostatin Analogues ◽  
Interferon Α ◽  
Peptide Receptor ◽  
Hepatic Arterial Embolization

AbstractNeuroendocrine tumors, or carcinoid tumors, of both the midgut and hindgut are quite rare, but their incidence is increasing. Surgery is the treatment of choice in patients who can tolerate an operation and have operable disease. Options for the treatment of metastatic disease include cytoreductive surgery, somatostatin analogues, interferon α, local liver therapies (hepatic arterial embolization, ablation), chemotherapy, Peptide-Receptor Radionucleotide Radiotherapy, angiogenesis inhibitors, and mammalian target of rapamycin inhibitors.

scholarly journals P-028 Role of somatostatin analogues in the treatment of neuroendocrine tumors (NETs), experience of Virgen de las Nieves University Hospital

2015 ◽  
Vol 26 ◽  
pp. iv8
Author(s):  
C. González-Rivas ◽  
L. Castillo ◽  
E. González-Flores ◽  
J. Ruiz-Vozmediano ◽  
L. Ochoa ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Somatostatin Analogues ◽  
University Hospital

scholarly journals Chemotherapy and role of the proliferation marker Ki-67 in digestive neuroendocrine tumors

2007 ◽  
Vol 14 (2) ◽  
pp. 221-232 ◽  
Author(s):  
Eduardo Vilar ◽  
Ramón Salazar ◽  
Jose Pérez-García ◽  
Javier Cortes ◽  
Kjell Öberg ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Retrospective Studies ◽  
Response To Treatment ◽  
Biological Behavior ◽  
Endocrine Tumors ◽  
Ki 67 ◽  
Pancreatic Endocrine Tumors ◽  
Poorly Differentiated ◽  
Selection For

Neuroendocrine tumors (NETs) of the digestive tract are a heterogeneous group of rare malignancies. Three major subgroups can be defined: pancreatic endocrine tumors, carcinoid tumors, and poorly differentiated gastroenteropancreatic NETs. Classically, digestive NETS have been considered to have an indolent course characterized for prolonged stabilizations or slow progressions, but there are clear differences in terms of aggressiveness, clinical course, and response to treatment among them. Retrospective studies have identified several clinicopathological and immunohistochemical factors as angioinvasion and proliferative index assessed by Ki-67 expression, which predict biological behavior and correlate with survival. Chemotherapy regimens based on the combination of several active drugs such as streptozocin, doxorubicin, 5-fluorouracil, dacarbazine, and temozolomide show low response rates, which sets the need to improve the results of the medical treatment of these malignancies. This review will analyze the role of Ki-67 in digestive NETs under a clinical perspective and will suggest future fields for development of this approach that enable a better patient selection for chemotherapy. Also a comprehensive review of the literature about chemotherapy in NETs is presented.

Drugs for the treatment of neuroendocrine tumours

2011 ◽  
Vol 152 (10) ◽  
pp. 379-391 ◽  
Author(s):  
Ágota Petrányi ◽  
György Bodoky
Keyword(s):  
Targeted Therapy ◽  
Neuroendocrine Tumors ◽  
Neuroendocrine Tumours ◽  
Somatostatin Analogues ◽  
Biologically Active ◽  
Somatostatin Analogue ◽  
Malignant Tumours ◽  
Phase 3 ◽  
Poorly Differentiated ◽  
Well Differentiated

Neuroendocrine tumours are heterogeneous and rare malignancies arising from endocrine cells located in various anatomical locations. Neuroendocrine tumours can be functional and may produce a wide variety of mediators, however, the majority of neuroendocrine tumours do not produce biologically active hormones (non-functioning tumours). On the basis of their pathological and biological characteristics they can be well differentiated as low malignant and poorly differentiated highly malignant tumours. In the case of the advanced low malignant tumours the application of somatostatin analogues not only may control symptoms but they also have direct anti-tumour effect. The use of higher doses of somatostatin analogues or new subtype selective agonists, and chimeric or pan-somatostatin analogues will probably improve the clinical management of the patients who fail to respond to standard somatostatin analogue treatment. Data show that somatostatin analogues and interferon have a synergistic effect. The currently used chemotherapy in progressive neuroendocrine tumors is mainly devoted to poorly differentiated tumours, but also to well differentiated carcinomas which are either not eligible or resistant to other therapies. However, the new anti-tumoural agents, could eventually replace these old recipes in the near future. Clinical trials show that telozomide with capecitabine result in more favorable toxic profile and higher and longer response rate in the case of well-differentiated tumours. Targeted therapy became a new possibility in neuroendocrine tumours too. The monoclonal antibody bevacizumab, which affects the vascular endothelial growth factor receptors, has beneficial effects both in monotherapies and in combination with somatostatin analogues or with oxaliplatine and capecitabine. Recently, the low molecular multikinase inhibitor, sunitinib has demonstrated efficacy in pancreas neuroendocrine tumors, which was proven in a phase 3 trial. The mammalian target of the rapamycin inhibitor everolimus, currently investigated in phase 3 trials, was also efficient in the same subtype. Further trials are needed to determine that in the case of other types of neuroendocrine tumours which targeted therapy could be efficient. Radioisotope-labeled peptide receptor therapy with 131I-MIBG, 90Y-DOTA-TOC or 177Lu-DOTA-TOC may offer a highly effective option for patients with progressive and advanced stage of neuroendocrine tumours. The purpose of this review is to review and analyze data available regarding contemporary chemotherapeutic management of neuroendocrine tumours in order to determine which therapy should be applied in the therapeutic arsenal. Orv. Hetil., 2011, 152, 379–391.

Role of Ca2+ and Na+ on luteinizing hormone release from the calf pituitary

1988 ◽  
Vol 255 (4) ◽  
pp. E469-E474
Author(s):  
J. P. Kile ◽  
M. S. Amoss
Keyword(s):  
Luteinizing Hormone ◽  
Ionophore A23187 ◽  
Channel Blockers ◽  
Hormone Release ◽  
Primary Cells ◽  
Rat Pituitary ◽  
Voltage Dependent ◽  
Lh Release ◽  
Ca2 Channels

It has been proposed that gonadotropin-releasing hormone (GnRH) stimulates Ca2+ entry by activation of voltage-independent, receptor-mediated Ca2+ channels in the rat gonadotroph. Little work has been done on the role of calcium in GnRH-induced luteinizing hormone (LH) release in species other than the rat. Therefore, this study was done to compare the effects of agents that alter Ca2+ or Na+ entry on LH release from calf anterior pituitary primary cells in culture. GnRH (100 ng/ml), Ca2+ ionophore A23187 (2.5 microM), and the depolarizing agent ouabain (0.1-10 microM) all produced significant increases (P less than 0.05) in LH release; these effects were significantly reduced when the cells were preincubated with the organic Ca2+ channel blockers nifedipine (1-10 microM) and verapamil (1-10 microM) and with Co2+ (0.01-1 mM). The effect of ouabain was inhibited by tetrodotoxin (TTX; 1-10 nM) as well as by nifedipine at 0.1-10 microM. In contrast to its effect on rat pituitary LH release, TTX significantly inhibited GnRH-stimulated LH release at 1-100 nM. These results suggest that GnRH-induced LH release may employ Ca2+ as a second messenger in bovine gonadotrophs and support recent speculation that GnRH-induced Ca2+ mobilization may in part be voltage dependent.

scholarly journals The Role of Circulating Biomarkers in Peripheral Arterial Disease

2021 ◽  
Vol 22 (7) ◽  
pp. 3601
Author(s):  
Goren Saenz-Pipaon ◽  
Esther Martinez-Aguilar ◽  
Josune Orbe ◽  
Arantxa González Miqueo ◽  
Leopoldo Fernandez-Alonso ◽  
...  
Keyword(s):  
Peripheral Arterial Disease ◽  
Lower Limb ◽  
Prediction Models ◽  
Arterial Disease ◽  
Cardiac Damage ◽  
Thrombotic Occlusion ◽  
Medical Treatments ◽  
Peripheral Arterial ◽  
Inflammatory Molecules

Peripheral arterial disease (PAD) of the lower extremities is a chronic illness predominantly of atherosclerotic aetiology, associated to traditional cardiovascular (CV) risk factors. It is one of the most prevalent CV conditions worldwide in subjects >65 years, estimated to increase greatly with the aging of the population, becoming a severe socioeconomic problem in the future. The narrowing and thrombotic occlusion of the lower limb arteries impairs the walking function as the disease progresses, increasing the risk of CV events (myocardial infarction and stroke), amputation and death. Despite its poor prognosis, PAD patients are scarcely identified until the disease is advanced, highlighting the need for reliable biomarkers for PAD patient stratification, that might also contribute to define more personalized medical treatments. In this review, we will discuss the usefulness of inflammatory molecules, matrix metalloproteinases (MMPs), and cardiac damage markers, as well as novel components of the liquid biopsy, extracellular vesicles (EVs), and non-coding RNAs for lower limb PAD identification, stratification, and outcome assessment. We will also explore the potential of machine learning methods to build prediction models to refine PAD assessment. In this line, the usefulness of multimarker approaches to evaluate this complex multifactorial disease will be also discussed.

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