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Clinical Cancer Research, ISSN 1078-0432, 05/2014, Volume 20, Issue 10, pp. 2651 - 2662
Purpose: To investigate the autocrine/endocrine role of Id1-induced insulin-like growth factor-II (IGF-II) in esophageal cancer, and evaluate the potential of... 
ACTIVATION | METASTASIS | CDNA MICROARRAY | ONCOLOGY | SIGNALING PATHWAY | PROSTATE-CANCER | SQUAMOUS-CELL CARCINOMA | GENE-EXPRESSION | GROWTH-FACTOR-II | ID-1 | TUMORS | Receptor, IGF Type 1 - metabolism | Receptor, IGF Type 1 - antagonists & inhibitors | Humans | Lung Neoplasms - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Insulin-Like Growth Factor II - immunology | Esophageal Neoplasms - pathology | Antibodies, Neutralizing - immunology | Insulin-Like Growth Factor II - genetics | Lung Neoplasms - secondary | RNA Interference | Esophageal Neoplasms - metabolism | Endocrine System - metabolism | Antimetabolites, Antineoplastic - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Autocrine Communication | Antibodies, Monoclonal - pharmacology | Antibodies, Neutralizing - pharmacology | Inhibitor of Differentiation Protein 1 - metabolism | Receptor, IGF Type 1 - genetics | Blotting, Western | Insulin-Like Growth Factor II - metabolism | Xenograft Model Antitumor Assays | Animals | Lung Neoplasms - prevention & control | Signal Transduction - drug effects | Tumor Burden - drug effects | Mice, Nude | Cell Line, Tumor | Inhibitor of Differentiation Protein 1 - genetics | Cell Proliferation - drug effects | Fluorouracil - pharmacology | Mice | Esophageal Neoplasms - drug therapy | Drug Resistance, Neoplasm - drug effects | Index Medicus
Journal Article
Journal of Hepatology, ISSN 0168-8278, 2010, Volume 52, Issue 4, pp. 550 - 559
Background & Aims IGF signaling has a relevant role in a variety of human malignancies. We analyzed the underlying molecular mechanisms of IGF signaling... 
Gastroenterology and Hepatology | IGF signaling | Hepatocellular carcinoma | A12 | Molecular therapy | miR-100 | SIGNALING PATHWAYS | RECEPTOR | MONOCLONAL-ANTIBODY | PROLIFERATION | FACTOR-II GENE | INSULIN | INHIBITION | GROWTH | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | MICRORNA | Receptor, IGF Type 1 - metabolism | Receptor, IGF Type 1 - antagonists & inhibitors | Humans | Gene Expression Regulation, Neoplastic | Hepatocytes - pathology | MicroRNAs - metabolism | Liver Neoplasms - therapy | Insulin Receptor Substrate Proteins - metabolism | Receptor, IGF Type 2 - metabolism | Receptor, IGF Type 2 - genetics | Insulin-Like Growth Factor II - genetics | Carcinoma, Hepatocellular - genetics | Insulin Receptor Substrate Proteins - genetics | Hepatocytes - physiology | Insulin-Like Growth Factor Binding Proteins - genetics | Liver Neoplasms - genetics | Antibodies, Monoclonal - pharmacology | Receptor, IGF Type 1 - genetics | Insulin-Like Growth Factor II - metabolism | Hep G2 Cells | Cell Division - physiology | Insulin-Like Growth Factor Binding Proteins - metabolism | Xenograft Model Antitumor Assays | Animals | Mice, Nude | Liver Neoplasms - metabolism | Receptor, IGF Type 1 - immunology | Insulin-Like Growth Factor Binding Protein 3 | Signal Transduction - physiology | Carcinoma, Hepatocellular - therapy | Mice | Mice, Inbred BALB C | Apoptosis - physiology | Carcinoma, Hepatocellular - metabolism | Liver cancer | Analysis | Transplantation of organs, tissues, etc | Hepatoma | Hepatitis C | Vascular endothelial growth factor | Endothelium | Protein binding | Index Medicus | molecular therapy | hepatocellular carcinoma
Journal Article
Journal of Molecular Cell Biology, ISSN 1674-2788, 2013, Volume 5, Issue 1, pp. 3 - 13
Dysregulation of microRNAs is a common feature in human cancers, including breast cancer (BC). Here we describe the epigenetic regulation of miR-148a and... 
DNMT1 | IGF-IR | IRS1 | tumor angiogenesis | breast cancer | miR-152 | miR-148a | PROMOTER HYPERMETHYLATION | METHYLATION | RECEPTOR | HUMAN BREAST-CANCER | CELL BIOLOGY | DNA METHYLTRANSFERASE 1 | EARLY EVENT | EXPRESSION | CARCINOMA | ENDOTHELIAL GROWTH-FACTOR | MICRORNA | Receptor, IGF Type 1 - metabolism | Cell Proliferation | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Phosphatidylinositol 3-Kinases - metabolism | Vascular Endothelial Growth Factor A - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Insulin Receptor Substrate Proteins - metabolism | Vascular Endothelial Growth Factor A - genetics | Breast Neoplasms - metabolism | DNA (Cytosine-5-)-Methyltransferases - metabolism | DNA Methylation | Neoplasm Grading | Cell Transformation, Neoplastic - genetics | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Adult | Female | Insulin Receptor Substrate Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Promoter Regions, Genetic | Signal Transduction | DNA (Cytosine-5-)-Methyltransferase 1 | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Receptor, IGF Type 1 - genetics | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Cell Line, Tumor | Neovascularization, Pathologic - genetics | Aged | MicroRNAs - genetics | Mitogen-Activated Protein Kinases - metabolism | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 08/2007, Volume 448, Issue 7157, pp. 1015 - 1021
Journal Article
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 1, pp. 58 - 71
Activation of the PI3K-AKT pathway in tumors is modulated by negative feedback, including mTORC1-mediated inhibition of upstream signaling. We now show that... 
RAPAMYCIN | TARGET | FORKHEAD TRANSCRIPTION FACTOR | CELLS | INSULIN-RECEPTOR | ACTIVATION | ONCOLOGY | SIGNALING PATHWAY | PHOSPHORYLATION | UPSTREAM | HUMAN CANCER | CELL BIOLOGY | RNA, Small Interfering - genetics | Receptor, IGF Type 1 - metabolism | Protein Binding - genetics | Receptor, ErbB-3 - metabolism | Humans | Forkhead Transcription Factors - metabolism | Protein Binding - drug effects | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Receptor, ErbB-2 - antagonists & inhibitors | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Quinoxalines - therapeutic use | Carcinoma, Non-Small-Cell Lung - metabolism | Receptor, ErbB-3 - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Breast Neoplasms - drug therapy | Receptor, IGF Type 1 - genetics | Signal Transduction - drug effects | Mice, Nude | Models, Biological | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | Feedback, Physiological - physiology | Quinazolines - pharmacology | Proteins - antagonists & inhibitors | Neoplasms - metabolism | Gene Expression - drug effects | Multiprotein Complexes | Receptor, ErbB-2 - metabolism | Promoter Regions, Genetic - genetics | Proto-Oncogene Proteins c-akt - genetics | Breast Neoplasms - metabolism | Mechanistic Target of Rapamycin Complex 1 | Quinoxalines - pharmacology | Receptor, Insulin - genetics | Female | Forkhead Transcription Factors - antagonists & inhibitors | Gene Expression Regulation, Neoplastic - drug effects | Drug Therapy, Combination | Gene Expression Regulation, Neoplastic - physiology | Carcinoma, Non-Small-Cell Lung - pathology | Up-Regulation - genetics | Forkhead Transcription Factors - genetics | Xenograft Model Antitumor Assays | Animals | Receptor Protein-Tyrosine Kinases - genetics | Breast Neoplasms - pathology | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Feedback, Physiological - drug effects | Receptor, Insulin - metabolism | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Benzylamines - pharmacology | Benzylamines - therapeutic use | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
Nature Communications, ISSN 2041-1723, 06/2017, Volume 8, Issue 1, pp. 15936 - 15936
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, pp. e61537 - e61537
Accumulating epidemiological evidence shows that obesity is associated with an increased risk of several types of adult cancers, including endometrial cancer.... 
BREAST-CANCER | TARGETED THERAPY | MULTIDISCIPLINARY SCIENCES | ENDOMETRIAL CANCER-CELLS | RESISTANCE | RISK | RECEPTOR GENE | MODEL | EXPRESSION | CHEMOTHERAPY | GROWTH-FACTOR-I | Cell Cycle - genetics | Receptor, IGF Type 1 - metabolism | Insulin-Like Growth Factor I - pharmacology | Metformin - therapeutic use | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Uterine Neoplasms - pathology | Humans | Cell Survival - genetics | Apoptosis - genetics | Glycogen Synthase Kinase 3 beta | Cystadenocarcinoma, Serous - pathology | Cystadenocarcinoma, Serous - drug therapy | Promoter Regions, Genetic - genetics | Uterine Neoplasms - enzymology | Receptor, Insulin - genetics | Adenylate Kinase - metabolism | Female | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Cell Survival - drug effects | Metformin - pharmacology | Tumor Suppressor Protein p53 - metabolism | Down-Regulation - drug effects | Glycogen Synthase Kinase 3 - metabolism | Receptor, IGF Type 1 - genetics | Cystadenocarcinoma, Serous - enzymology | Cell Movement - drug effects | Insulin - metabolism | Signal Transduction - drug effects | Uterine Neoplasms - drug therapy | Cell Line, Tumor | Endometrial Neoplasms - pathology | Receptor, Insulin - metabolism | Cell Proliferation - drug effects | Forkhead Box Protein O1 | Cell Cycle - drug effects | Forkhead Transcription Factors | Insulin-Like Growth Factor I - metabolism | Type 2 diabetes | Obesity | Carcinoma | Endometrial cancer | Insulin resistance | Metformin | Tumor proteins | Health aspects | Epidemiology | Diabetes therapy | Cancer | Cell proliferation | Hyperinsulinemia | Insulin-like growth factor I | p53 Protein | Insulin-like growth factors | Kinases | Cancer therapies | Ovarian cancer | Signal transduction | Cell growth | Pathways | Uterus | Growth factors | Endometrium | Diabetes mellitus | Health risks | Insulin | Signaling | Cell lines | Cell migration | Apoptosis | Index Medicus
Journal Article