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BMC CANCER, ISSN 1471-2407, 09/2019, Volume 19, Issue 1, pp. 893 - 8
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 12, p. e15200
Journal Article
BMC Cancer, ISSN 1471-2407, 06/2019, Volume 19, Issue 1, pp. 575 - 8
BackgroundDistant metastases frequently occur in gastroenteropancreatic neuroendocrine tumors. If hepatic surgery is not feasible, patients are treated with... 
Intra-individual | microRNA | Somatostatin | Neuroendocrine tumor | MANAGEMENT | NEOPLASMS | ENETS CONSENSUS GUIDELINES | ENDOCRINE | MIRNA EXPRESSION | ONCOLOGY | COLORECTAL-CANCER | MICRORNA EXPRESSION | LANREOTIDE | Medicine, Experimental | Medical research | Research | Gene expression
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2017, Volume 12, Issue 8, p. e0182852
Background/Aims The therapeutic options for metastatic neuroendocrine tumors (NETs) are limited. As PI3K signaling is often activated in NETs, we have assessed... 
MAMMALIAN TARGET | CARCINOMA-CELLS | SIGNALING PATHWAYS | MULTIDISCIPLINARY SCIENCES | GLYCOGEN-SYNTHASE KINASE-3 | IN-VIVO | PANCREATIC-CANCER | GROWTH | P110-ALPHA ISOFORM | CHROMOGRANIN-A | MTOR | Caspase 7 - metabolism | Class I Phosphatidylinositol 3-Kinases - genetics | Class I Phosphatidylinositol 3-Kinases - metabolism | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | Gene Expression Regulation, Neoplastic | Proto-Oncogene Proteins c-akt - genetics | Dose-Response Relationship, Drug | Receptors, Somatostatin - genetics | Caspase 3 - genetics | Antineoplastic Agents - pharmacology | Chromogranin A - metabolism | Receptors, Somatostatin - metabolism | Chromogranin A - genetics | Proto-Oncogene Proteins c-akt - metabolism | Everolimus - pharmacology | Signal Transduction | Caspase 7 - genetics | Pancreas - drug effects | Pancreas - pathology | Pancreas - metabolism | Glycogen Synthase Kinase 3 - metabolism | Class I Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Drug Synergism | Glycogen Synthase Kinase 3 - genetics | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Cell Cycle - drug effects | Cell culture | Biotechnology | Flow cytometry | Thoracic surgery | Transcription | Peptides | AKT protein | Activation | Metastasis | Kinases | Assaying | Cancer therapies | Western blotting | Metastases | Receptors | Cell activation | Cell growth | Surgery | Gastroenterology | Cell cycle | Inhibition | Somatostatin | Pancreas | Enzyme-linked immunosorbent assay | Internal medicine | Secretion | Colonies | Metabolism | 1-Phosphatidylinositol 3-kinase | Medicine | Sensitivity | Chemotherapy | Nets | Cell lines | Stem cells | Umbilical cord | Differentiation | Viability | Endocrinology | Somatostatin receptors | Tumors | Neuroendocrine tumors | Apoptosis
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2015, Volume 10, Issue 12, p. e0143830
Background The mTORC1-inhibitor everolimus shows limited efficacy in treating patients with gastro-entero-pancreatic or pulmonary neuroendocrine tumors (NETs),... 
CELL LUNG-CANCER | GROWTH-FACTOR RECEPTOR | HEPATOCELLULAR-CARCINOMA | MULTIDISCIPLINARY SCIENCES | RESISTANCE | AGENTS | GLYCOSYLATION | MODEL | SORAFENIB | STATINS | LINES | Neoplasms - metabolism | Receptor, Epidermal Growth Factor - genetics | Everolimus - pharmacology | Lovastatin - pharmacology | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Humans | Ribosomal Protein S6 Kinases, 70-kDa - genetics | Proto-Oncogene Proteins c-akt - genetics | Hep G2 Cells | Mice, Knockout | Neoplasms - drug therapy | Drug Synergism | Lovastatin - agonists | Receptor, Epidermal Growth Factor - metabolism | Animals | MAP Kinase Signaling System - drug effects | Neoplasms - genetics | Mice | Proto-Oncogene Proteins c-akt - metabolism | Everolimus - agonists | Lovastatin | Dosage and administration | Drugs | Cell culture | Biotechnology | Pheochromocytoma | Midgut | Hepatocellular carcinoma | AKT protein | Activation | Metastasis | Kinases | Cancer therapies | Anticancer properties | Liver cancer | Signal transduction | Epidermal growth factor | Pathways | Rodents | Penicillin | Attenuation | Inhibition | Pancreas | Drug dosages | Medical research | Epidermal growth factor receptors | Extracellular signal-regulated kinase | Patients | Signaling | Hypotheses | Cell lines | Aberration | Viability | Tumors | Neuroendocrine tumors
Journal Article
Cancer Letters, ISSN 0304-3835, 2010, Volume 295, Issue 1, pp. 100 - 109
Abstract Several studies have established a link between aberrant PI(3)K–Akt–mTOR- and Ras–Raf–MEK–Erk1/2 signaling and neuroendocrine tumor disease. In this... 
Hematology, Oncology and Palliative Medicine | G0/G1 arrest | Ras–Raf–MEK–Erk1/2 signaling | PIK–Akt–mTOR signaling | Small-molecule inhibitor | Neuroendocrine tumors | Apoptosis | Ras-Raf-MEK-Erk1/2 signaling | PIK-Akt-mTOR signaling | CANCER-CELLS | RAF/MEK/ERK | ANGIOGENESIS | PHOSPHORYLATION | KINASE | SUNITINIB MALATE | FACTOR RECEPTOR | RAD001 EVEROLIMUS | ONCOLOGY | PATHWAY | ENDOTHELIAL GROWTH-FACTOR | Phosphorylation | raf Kinases - antagonists & inhibitors | Humans | Phosphatidylinositol 3-Kinases - metabolism | Vascular Endothelial Growth Factor A - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | G1 Phase - drug effects | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | raf Kinases - metabolism | Quinolines - pharmacology | Dose-Response Relationship, Drug | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Everolimus | Cell Survival - drug effects | Sirolimus - analogs & derivatives | Neuroendocrine Tumors - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | Imidazoles - pharmacology | Pyrimidines - pharmacology | Sirolimus - pharmacology | Pyrroles - pharmacology | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Cell Line, Tumor | Neuroendocrine Tumors - drug therapy | Feedback, Physiological - drug effects | TOR Serine-Threonine Kinases | Proteins | Studies | Cell culture | Cell growth | Feedback | Kinases | Tumors
Journal Article
Journal Article
Journal Article