Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P39060 (endostatin)
 2,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic neuroendocrine tumors (NETs) consist of a wide group of neoplasms, with different biological behaviors in terms of aggressiveness and hormone production. In the last two decades, significant progress has been observed in our understanding of their biology, diagnosis and treatment. Surgery remains to be the only curative approach, but unfortunately the diagnosis is often delayed due to the slow growth of these tumors and the difficulty in identifying the symptoms related to the tumor-released hormones. In addition to surgery, other approaches to control the disease are biological therapy consisting of somatostatin analogs and interferon (IFN), systemic chemotherapy, radioligand therapy and local therapy with chemoembolization. Several newer cytotoxic agents, including irinotecan, gemcitabine, taxanes, oxaliplatin, capecitabine and PS-341 have been studied in metastatic patients. Considering the high vascularity of these tumors, antiangiogenic agents like endostatin and thalidomide have also been evaluated in advanced NETs. Although these agents seem to have potential activity in NETs and may increase progression free survival, none of these currently available medical therapeutic options are curative. While more efficient novel strategies are to be developed, the rationale use of the current therapeutic options may improve quality of life, control the symptoms related to the hypersecretion of hormones and/or peptides, control tumor proliferation and prolong survival in patients suffering from NETs.
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PMID:Current medical treatment of pancreatic neuroendocrine tumors. 1741 76

Hepatocellular carcinoma (HCC) is a hypervascular tumor, and tumor progression and prognosis is associated with angiogenesis. Extracellular matrix remodeling and inflammation play important roles in hepatocarcinogenesis. Some ingredients of extracellular matrix such as endostatin and sulfated polysaccharide, some immunomodulatory agents and cox-2 inhibitor suppress the angiogenesis of HCC. Because vasculogenic mimicry is associated with high tumor grade, some differentiation agents are used to inhibit antiagiogenesis. Besides suppressing the proliferation directly, somatostatin inhibits angiogenesis to suppress growth indirectly. Copper chelator prevents copper from functioning as a cofactor in angiogenesis. The renin-angiotensin system is frequently activated in patients with chronic liver diseases. Perindopril, an angiotensin converting enzyme inhibitor, inhibits angiogenesis by reducing vascular endothelial growth factor (VEGF) production. Kinase inhibitors of VEGF and epidermal growth factor receptors are expected to be of benefit for some patients. Following transarterial embolisation and/or resection, antiangiogenic therapy could prevent the recurring and metastasis. Hypoxia enhances the proliferation, suppresses the differentiation and apoptosis, and induces multidrug resistance of HCC. Because antiangiogenic therapies induce hypoxia, it should be borne in mind the side affects of antiangiogenic therapy. Because long-acting antiangiogenent are needed to control cancer, it needs more clinical studies to confirm the drug resistance of antiangiogenetic therapy.
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PMID:New strategy of antiangiogenic therapy for hepatocellular carcinoma. 1899 74

Lung cancer encompasses a diverse spectrum of histologic subtypes. Until recently, the majority of therapeutic advances were limited to the minority of patients with adenocarcinoma. With the advent of comprehensive genomic profiling of squamous and small cell lung cancers, new therapeutic targets have emerged. For squamous tumors, the most promising of these include fibroblast growth factor receptor (FGFR), the phosphatidylinositol 3-kinase (PI3K) pathway, discoidin domain receptor 2 (DDR2), and G1/S checkpoint regulators. In 2014, the antiangiogenic agent ramucirumab was approved for all non-small cell lung cancer (NSCLC) histologies, including squamous tumors. Immunotherapeutic approaches also appear to be promising for these cases. Genomic analysis of small cell lung cancer has revealed a high mutation burden, but relatively few druggable driver oncogenic alterations. Current treatment strategies under investigation are focusing on targeting mitotic, cell cycle, and DNA repair regulation, as well as immunotherapy. Pulmonary neuroendocrine tumors represent a diverse spectrum of diseases that may be treated with somatostatin analogs, cytotoxic agents, and molecularly targeted therapies. Radiolabeled somatostatin analogs and combinations with mammalian target of rapamycin (mTOR) inhibitors also show potential. Large cell neuroendocrine tumors share numerous clinical, pathologic, and molecular features with small cell lung cancer; however, whether they should be treated similarly or according to a NSCLC paradigm remains a matter of debate.
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PMID:Beyond adenocarcinoma: current treatments and future directions for squamous, small cell, and rare lung cancer histologies. 2599 53

Neuroendocrine tumors (NETs) are heterogeneous malignancies arising from the diffuse neuroendocrine system. They frequently originate in the gastroenteropancreatic (GEP) tract and the bronchopulmonary tree, and their incidence has steadily increased in the last 3 decades. Fundamental biologic and genomic differences underlie the clinical heterogeneity of NETs, and distinct molecular features characterize NETs of different grades and different primary sites. Although surgery remains the cornerstone of treatment for localized tumors, systemic treatment options for patients with metastatic NETs have expanded considerably. Somatostatin analogs have demonstrated both antisecretory and antitumor efficacy. Peptide receptor radionuclide therapy with lutetium-177 dotatate (177 Lu-DOTATATE) has been approved for advanced GEP-NETs. The antitumor activity of everolimus has been demonstrated across a wide spectrum of NETs, and the antiangiogenic agent sunitinib has been approved for pancreatic NETs (pNETs). Chemotherapy with temozolomide and capecitabine has recently demonstrated an unprecedented prolongation of progression-free survival in a randomized trial of pNETs. Multiple retrospective series have reported the efficacy of liver-directed therapies both for palliating symptoms of hormone excess and for controlling tumor growth. Telotristat, an oral inhibitor of tryptophan hydroxylase, has been shown to reduce diarrhea in patients with carcinoid syndrome. Defining the therapeutic algorithm and identifying biomarkers predictive of response to treatments are among the main priorities for the next decade of research in the NET field.
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PMID:Gastroenteropancreatic Neuroendocrine Tumors. 3029 30