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Cancer, ISSN 0008-543X, 10/2014, Volume 120, Issue 19, pp. 2980 - 2985
BACKGROUND Targeting a single pathway in pancreatic adenocarcinoma (PC) is unlikely to affect its natural history. We tested the hypothesis that simulataneous... 
pancreatic cancer | erlotinib signaling | randomized phase II | IGF‐1R | cixutumumab | EGFR | targeted treatment | Erlotinib signaling | Targeted treatment | Randomized phase II | Pancreatic cancer | Cixutumumab | IGF-1R | CARCINOMA-CELLS | DUCTAL ADENOCARCINOMA | MONOCLONAL-ANTIBODY | SINGLE-AGENT CETUXIMAB | BREAST-CANCER | INHIBITION | K-RAS | ONCOLOGY | THERAPEUTIC TARGET | C-MET | RESISTANCE | Erlotinib Hydrochloride | Pancreatic Neoplasms - metabolism | Humans | Middle Aged | Antibodies, Monoclonal - adverse effects | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Receptor, Epidermal Growth Factor - drug effects | Male | Insulin-Like Growth Factor I - drug effects | Pancreatic Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - metabolism | Adenocarcinoma - metabolism | Adult | Deoxycytidine - adverse effects | Female | Quinazolines - administration & dosage | Drug Administration Schedule | Deoxycytidine - administration & dosage | Pancreatic Neoplasms - pathology | Kaplan-Meier Estimate | Treatment Outcome | Adenocarcinoma - drug therapy | Adenocarcinoma - secondary | Disease-Free Survival | Signal Transduction - drug effects | Antibodies, Monoclonal - administration & dosage | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Quinazolines - adverse effects | Aged | Deoxycytidine - analogs & derivatives | Insulin-Like Growth Factor I - metabolism | Index Medicus | Abridged Index Medicus
Journal Article
Journal Article
The Journal of Clinical Endocrinology & Metabolism, ISSN 0021-972X, 09/2017, Volume 102, Issue 9, pp. 3480 - 3490
CONTEXT:Depending on its lipolytic activity, glucagon plays a promising role in obesity treatment. Glucagon-induced growth hormone (GH) release can promote its... 
FOXO | STIMULATION | GROWTH-HORMONE | GHRELIN | ENDOCRINOLOGY & METABOLISM | SECRETION | SUPPRESSION | EXPRESSION | AXIS | Humans | Insulin-Like Growth Factor Binding Proteins - drug effects | Diabetes Mellitus, Type 1 - metabolism | Glucagon - administration & dosage | Male | Insulin-Like Growth Factor I - drug effects | Forkhead Box Protein O1 - drug effects | Dose-Response Relationship, Drug | Statistics, Nonparametric | Adult | Female | Forkhead Box Protein O1 - metabolism | Double-Blind Method | Drug Administration Schedule | Enzyme-Linked Immunosorbent Assay | Growth Hormone - drug effects | Growth Hormone - metabolism | Obesity - physiopathology | Injections, Intramuscular | Blotting, Western | Diabetes Mellitus, Type 1 - drug therapy | Obesity - metabolism | Insulin-Like Growth Factor Binding Proteins - metabolism | Diabetes Mellitus, Type 1 - diagnosis | Insulin-Like Growth Factor I - metabolism | TOR protein | Phosphorylation | Glucagon | Insulin-like growth factor I | Insulin-like growth factor-binding protein 2 | Insulin-like growth factor-binding protein 1 | AKT protein | Insulin-like growth factors | Kinases | Proteins | Biomedical materials | Reduction | FOXO1 protein | Osteosarcoma | Forkhead protein | Insulin-like growth factor-binding protein 3 | Biocompatibility | Lipid metabolism | Protein transport | Translocation | Obesity | Secretion | Diabetes mellitus | Rapamycin | Osteosarcoma cells | Gene expression | Metabolism | Insulin | Biological activity | Nuclear transport | Hepatocytes | Growth hormone
Journal Article
Molecular and Cellular Neuroscience, ISSN 1044-7431, 2005, Volume 29, Issue 3, pp. 381 - 393
‘Protective autoimmunity’ refers to a well-controlled anti-self response that helps the body resist neurodegeneration. The response is mediated by autoimmune T... 
PROINFLAMMATORY CYTOKINE | NEUROPROTECTIVE AUTOIMMUNITY | MULTIPLE-SCLEROSIS | ALZHEIMERS-DISEASE | MACROPHAGES | GLUTAMATE | CENTRAL-NERVOUS-SYSTEM | SELF-ANTIGEN | NEUROSCIENCES | T-CELLS | GROWTH-FACTOR-I | Amyloid beta-Peptides - pharmacology | Gliosis - therapy | Transcriptional Activation - drug effects | Gliosis - physiopathology | Hippocampus - drug effects | Lipopolysaccharides - antagonists & inhibitors | Insulin-Like Growth Factor I - drug effects | Neurodegenerative Diseases - immunology | Lipopolysaccharides - immunology | Histocompatibility Antigens Class II - drug effects | Insulin-Like Growth Factor I - immunology | Interleukin-4 - pharmacology | Lymphocyte Activation - immunology | Encephalitis - physiopathology | Microglia - immunology | Autoimmunity - immunology | T-Lymphocytes - drug effects | Tumor Necrosis Factor-alpha - immunology | Gliosis - immunology | Organ Culture Techniques | Animals, Newborn | Cell Line | Encephalitis - therapy | Hippocampus - immunology | Microglia - drug effects | Cells, Cultured | Rats | Encephalitis - immunology | Neurodegenerative Diseases - therapy | Down-Regulation - drug effects | Rats, Sprague-Dawley | Interleukin-4 - immunology | Amyloid beta-Peptides - antagonists & inhibitors | Animals | Histocompatibility Antigens Class II - immunology | Neurodegenerative Diseases - physiopathology | Tumor Necrosis Factor-alpha - drug effects | Down-Regulation - immunology | Lymphocyte Activation - drug effects | Interferon-gamma - immunology | Lipopolysaccharides - pharmacology | Amyloid beta-Peptides - immunology | T-Lymphocytes - immunology | Transcriptional Activation - physiology | Hippocampus - physiopathology | Autoimmunity - drug effects | Interferon-gamma - pharmacology
Journal Article
Journal Article
Journal Article
Endocrinology, ISSN 0013-7227, 07/2015, Volume 156, Issue 7, pp. 2395 - 2408
Medulloblastoma (Med) is the most common malignant brain tumor in children. The role of ESR2 [estrogen receptor (ER)-β] in promoting Med growth was... 
BREAST-CANCER | MUTANT MICE | RAT CEREBELLUM | ER-BETA | PROTEIN-KINASE | HETEROZYGOUS MICE | ENDOCRINOLOGY & METABOLISM | FACTOR-I | NEUROPROTECTION | CEREBELLAR GRANULE CELLS | BRAIN-TUMORS | Receptor, IGF Type 1 - metabolism | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | Apoptosis - genetics | Male | Insulin-Like Growth Factor I - genetics | Insulin-Like Growth Factor I - drug effects | RNA, Messenger - metabolism | Tumor Suppressor Protein p53 - genetics | Estrogen Receptor beta - metabolism | Insulin-Like Growth Factor II - drug effects | Proto-Oncogene Proteins c-bcl-2 - metabolism | Estrogen Receptor beta - genetics | Insulin-Like Growth Factor II - genetics | Receptor, IGF Type 1 - drug effects | Female | Gene Expression Regulation, Neoplastic - drug effects | Patched Receptors | Medulloblastoma - genetics | Estradiol - pharmacology | Gene Expression Regulation, Neoplastic - genetics | RNA, Messenger - drug effects | Up-Regulation - genetics | Medulloblastoma - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Receptor, IGF Type 1 - genetics | Insulin-Like Growth Factor II - metabolism | Mice, Knockout | Up-Regulation - drug effects | Animals | Proto-Oncogene Proteins c-bcl-2 - drug effects | Cell Line, Tumor | Mice | Insulin-Like Growth Factor I - metabolism | Patched-1 Receptor | Receptors, Cell Surface - genetics | Original Research
Journal Article
Gynecologic Oncology, ISSN 0090-8258, 2016, Volume 143, Issue 3, pp. 466 - 471
Abstract Objective Metformin reduces cancer incidence and improves overall survival in diabetic patients. In preclinical studies, metformin decreases... 
Hematology, Oncology and Palliative Medicine | Obstetrics and Gynecology | mTOR | Metformin | Inhibition | Endometrial cancer | Window of opportunity | RISK | PROLIFERATION | OBSTETRICS & GYNECOLOGY | DIABETIC-PATIENTS | BREAST-CANCER | TRIAL | THERAPY | ONCOLOGY | COHORT | NEOADJUVANT | Immunohistochemistry | AMP-Activated Protein Kinases - metabolism | Phosphoproteins - drug effects | Prospective Studies | Apoptosis - drug effects | Humans | Leptin - metabolism | Middle Aged | Caspase 3 - metabolism | Endometrial Neoplasms - metabolism | Endometrium - drug effects | Ki-67 Antigen - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Insulin-Like Growth Factor I - drug effects | Phosphoproteins - metabolism | AMP-Activated Protein Kinases - drug effects | Carcinoma, Endometrioid - metabolism | Mitogen-Activated Protein Kinase 3 - drug effects | Lectins - metabolism | Phosphatidylinositol 3-Kinases - drug effects | Caspase 3 - drug effects | Biomarkers, Tumor - metabolism | Adult | Female | Proto-Oncogene Proteins c-akt - metabolism | Endometrium - metabolism | Cytokines - metabolism | GPI-Linked Proteins - drug effects | Metformin - pharmacology | GPI-Linked Proteins - metabolism | Hypoglycemic Agents - pharmacology | Insulin - metabolism | Cytokines - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Lectins - drug effects | Endometrial Neoplasms - pathology | Aged | Cell Proliferation - drug effects | Endometrium - pathology | Carcinoma, Endometrioid - pathology | Insulin-Like Growth Factor I - metabolism | Ki-67 Antigen - drug effects | Proto-Oncogene Proteins c-akt - drug effects | Women | Diabetics | Analysis | Oncology, Experimental | Research | Cancer
Journal Article
European Journal of Endocrinology, ISSN 0804-4643, 10/2014, Volume 171, Issue 4, pp. 471 - 479
Journal Article
14.