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1. Full Text SUMOylation regulates AKT1 activity
by De La Cruz-Herrera, C.F and Campagna, M and Lang, V and Del Carmen González-Santamaría, J and Marcos-Villar, L and Rodríguez, M.S and Vidal, A and Collado, M and Rivas, C
Oncogene, ISSN 0950-9232, 03/2015, Volume 34, Issue 11, pp. 1442 - 1450
Serine threonine kinase AKT has a central role in the cell, controlling survival, proliferation, metabolism and angiogenesis. Deregulation of its activity... 
ACTIVATION | QUANTITATIVE PROTEOMICS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEAT-SHOCK | ONCOGENIC TRANSFORMATION | SUMO-1 MODIFICATION | PROTEIN-KINASE B | PML | CELL BIOLOGY | ONCOLOGY | PATHWAY | GENETICS & HEREDITY | NIH3T3 CELLS | Phosphorylation | Cell Proliferation | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Cercopithecus aethiops | Apoptosis - genetics | Sumoylation - physiology | Proto-Oncogene Proteins c-akt - genetics | MCF-7 Cells | HEK293 Cells | Female | Proto-Oncogene Proteins c-akt - metabolism | Ubiquitins - metabolism | Sumoylation - genetics | Signal Transduction | Small Ubiquitin-Related Modifier Proteins - metabolism | Animals | Cell Line, Tumor | Mice | SUMO-1 Protein - metabolism | Enzyme Activation | HeLa Cells | Mutation | Neoplasms - pathology | COS Cells | 3T3 Cells | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Ubiquitin | Cell proliferation | Analysis | Physiological aspects | Genetic aspects | Research | Protein kinases | Angiogenesis | Kinases | Metabolism | Cancer
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2. Full Text An NF-κB pathway-mediated positive feedback loop amplifies Ras activity to pathological levels in mice
by Daniluk, Jaroslaw and Liu, Yan and Deng, Defeng and Chu, Jun and Huang, Haojie and Gaiser, Sebastian and Cruz-Monserrate, Zobeida and Wang, Huamin and Ji, Baoan and Logsdon, Craig D
Journal of Clinical Investigation, ISSN 0021-9738, 04/2012, Volume 122, Issue 4, pp. 1519 - 1528
Genetic mutations that give rise to active mutant forms of Ras are oncogenic and found in several types of tumor. However, such mutations are not clear... 
SIGNAL-TRANSDUCTION | PROTEASE INHIBITOR | MEDICINE, RESEARCH & EXPERIMENTAL | PANCREATIC DUCTAL ADENOCARCINOMA | ACTIVATION | K-RAS | ONCOGENIC KRAS | MOUSE MODEL | IN-VIVO | ACINAR-CELLS | CANCER | Inflammation - chemically induced | Pancreatic Neoplasms - metabolism | Pancreatic Neoplasms - etiology | Humans | Carcinoma, Pancreatic Ductal - metabolism | Sincalide - toxicity | Pancreatitis, Chronic - chemically induced | Proto-Oncogene Proteins p21(ras) - physiology | Gabexate - toxicity | I-kappa B Kinase - physiology | Carcinoma, Pancreatic Ductal - genetics | Cyclooxygenase 2 - biosynthesis | Inflammation - complications | Inflammation - metabolism | Cell Transformation, Neoplastic - genetics | Inflammation Mediators - metabolism | Carcinoma, Pancreatic Ductal - etiology | Gene Expression Regulation, Neoplastic - physiology | I-kappa B Kinase - deficiency | Lipopolysaccharides - toxicity | Cyclooxygenase 2 Inhibitors - pharmacology | Neoplasm Proteins - biosynthesis | Pancreatic Neoplasms - pathology | Ceruletide - toxicity | Enzyme Induction | Cyclooxygenase 2 - physiology | Gabexate - analogs & derivatives | Mice, Transgenic | Pancreatic Neoplasms - genetics | I-kappa B Kinase - genetics | Pancreas - metabolism | Pancreatitis, Chronic - genetics | Carcinoma, Pancreatic Ductal - pathology | Precancerous Conditions - genetics | Proto-Oncogene Proteins p21(ras) - biosynthesis | Gene Knock-In Techniques | Animals | NF-kappa B - physiology | Inflammation - genetics | Mice | Feedback, Physiological - physiology | Precancerous Conditions - chemically induced | Genes, ras | Pancreatitis, Chronic - metabolism
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3. Full Text SNX2112, a Synthetic Heat Shock Protein 90 Inhibitor, Has Potent Antitumor Activity against HER Kinase–Dependent Cancers
by Sarat Chandarlapaty and Ayana Sawai and Qing Ye and Anisa Scott and Melanie Silinski and Ken Huang and Pat Fadden and Jeff Partdrige and Steven Hall and Paul Steed and Larry Norton and Neal Rosen and David B. Solit
Clinical Cancer Research, ISSN 1078-0432, 01/2008, Volume 14, Issue 1, pp. 240 - 248
Purpose: The heat shock protein 90 (Hsp90) chaperone plays an important role in transformation by regulating the conformational maturation and stability of... 
HSP90 | breast cancer | 17-AAG | Geldanamycin | HER2 | HSP90 INHIBITORS | PROTEIN | ANSAMYCINS | ONCOLOGY | PHASE-I TRIAL | GELDANAMYCIN | 17-ALLYLAMINO-17-DEMETHOXYGELDANAMYCIN | GROWTH-FACTOR RECEPTORS | DEGRADATION | ONCOGENIC TRANSFORMATION | B-RAF | Extracellular Signal-Regulated MAP Kinases - drug effects | Humans | Immunoblotting | Lactams, Macrocyclic - pharmacology | Benzoquinones - pharmacokinetics | Benzoquinones - pharmacology | Xenograft Model Antitumor Assays | Animals | Lactams, Macrocyclic - pharmacokinetics | Prodrugs - pharmacokinetics | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Mice, Nude | Cell Line, Tumor | Female | Antineoplastic Agents - pharmacokinetics | Antineoplastic Agents - pharmacology | Cell Proliferation - drug effects | Mice | Receptor, ErbB-2 - drug effects | Neoplasms, Experimental - drug therapy | Prodrugs - pharmacology
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4. Full Text Obstacles Posed by the Tumor Microenvironment to T cell Activity: A Case for Synergistic Therapies
by Anderson, Kristin G and Stromnes, Ingunn M and Greenberg, Philip D
Cancer Cell, ISSN 1535-6108, 03/2017, Volume 31, Issue 3, pp. 311 - 325
T cell dysfunction in solid tumors results from multiple mechanisms. Altered signaling pathways in tumor cells help produce a suppressive tumor... 
adoptive T cell therapy | tumor microenvironment | TME | T cell dysfunction | genetic engineering | immunotherapy | INTERLEUKIN-8 EXPRESSION | ONCOLOGY | ONCOGENIC KRAS | INDOLEAMINE 2,3-DIOXYGENASE | RECEPTOR EXPRESSION | FATTY-ACID SYNTHASE | FOCAL ADHESION KINASE | PROGNOSTIC-SIGNIFICANCE | ANTITUMOR-ACTIVITY | WNT/BETA-CATENIN PATHWAY | HUMAN PANCREATIC-CANCER | CELL BIOLOGY | Neoplasms - metabolism | Humans | Lactic Acid - metabolism | Tumor Microenvironment | Receptors, Antigen, T-Cell - physiology | Amino Acids - metabolism | Genes, p53 | Neoplasms - therapy | Neoplasms - immunology | Glucose - metabolism | T-Lymphocytes - immunology | Fatty Acids - metabolism | Cytotoxicity, Immunologic | Medical colleges | Antigens | Melanoma | Development and progression | T cells | Cancer | Ovarian cancer | Medical research | Immunotherapy | Medicine, Experimental
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5. Full Text Blockade of the MEK/ERK signalling cascade by AS703026, a novel selective MEK1/2 inhibitor, induces pleiotropic anti‐myeloma activity in vitro and in vivo
by Kim, Kihyun and Kong, Sun‐Young and Fulciniti, Mariateresa and Li, Xianfeng and Song, Weihua and Nahar, Sabikun and Burger, Peter and Rumizen, Mathew J and Podar, Klaus and Chauhan, Dharminder and Hideshima, Teru and Munshi, Nikhil C and Richardson, Paul and Clark, Ann and Ogden, Janet and Goutopoulos, Andreas and Rastelli, Luca and Anderson, Kenneth C and Tai, Yu‐Tzu
British Journal of Haematology, ISSN 0007-1048, 05/2010, Volume 149, Issue 4, pp. 537 - 549
Summary This study investigated the cytotoxicity and mechanism of action of AS703026, a novel, selective, orally bioavailable MEK1/2 inhibitor, in human... 
bone marrow stromal cells (BMSCs) | novel kinase inhibitor therapy | multiple myeloma (MM) | MEK1/2 inhibitor | Bone marrow stromal cells (BMSCs) | Novel kinase inhibitor therapy | Multiple myeloma (MM) | GENE-MUTATIONS | N-RAS | BONE-MARROW | 2 inhibitor | BRAF GENE | ACTIVATING RAS MUTATIONS | PROTEIN-KINASE CASCADE | ONCOGENIC RAS | VEGF SECRETION | MEK1 | PLASMA-CELL LEUKEMIA | HEMATOLOGY | HUMAN MULTIPLE-MYELOMA | Niacinamide - analogs & derivatives | MAP Kinase Kinase 1 - antagonists & inhibitors | Apoptosis - drug effects | Humans | Niacinamide - therapeutic use | Mice, SCID | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Dose-Response Relationship, Drug | Xenograft Model Antitumor Assays | Multiple Myeloma - drug therapy | Multiple Myeloma - pathology | Animals | MAP Kinase Signaling System - drug effects | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Antineoplastic Agents - pharmacology | Mice | Protein Kinase Inhibitors - pharmacology | Cell Death - drug effects | Niacinamide - pharmacology | Tumor Cells, Cultured | Cell research | Dexamethasone | Sugars | Multiple myeloma | Tumors | Monosaccharides
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6. Full Text HOTAIR is a negative prognostic factor and exhibits pro-oncogenic activity in pancreatic cancer
by Kim, K and Jutooru, I and Chadalapaka, G and Johnson, G and Frank, J and Burghardt, R and Kim, S and Safe, S
Oncogene, ISSN 0950-9232, 03/2013, Volume 32, Issue 13, pp. 1616 - 1625
HOTAIR is a long intervening non-coding RNA (lincRNA) that associates with the Polycomb Repressive Complex 2 (PRC2) and overexpression is correlated with poor... 
HOTAIR | Cell cycle progression | Pro-oncogenic | Invasion | Prognostic | ACTIVATION | pro-oncogenic | PROTEIN | CHROMATIN | DUCTAL ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | MECHANISMS | CELL BIOLOGY | prognostic | INTERFERON | invasion | LONG NONCODING RNA | REPRESSION | ONCOLOGY | GENETICS & HEREDITY | GENE-EXPRESSION | cell cycle progression | MIRNAS | Prognosis | Pancreatic Neoplasms - diagnosis | Humans | Transplantation, Heterologous | RNA, Long Noncoding - physiology | Carcinoma, Pancreatic Ductal - genetics | Gene Knockdown Techniques | Cell Transformation, Neoplastic - genetics | Biomarkers, Tumor - metabolism | Carcinoma, Pancreatic Ductal - diagnosis | Female | Gene Expression Regulation, Neoplastic - drug effects | Gene Expression Regulation, Neoplastic - physiology | Pancreatic Neoplasms - pathology | RNA, Small Interfering - pharmacology | Pancreatic Neoplasms - genetics | Biomarkers, Tumor - physiology | RNA, Long Noncoding - genetics | Carcinoma, Pancreatic Ductal - pathology | Animals | Cell Line, Tumor | Biomarkers, Tumor - genetics | Cell Proliferation - drug effects | Mice | Cell Transformation, Neoplastic - drug effects | RNA, Long Noncoding - antagonists & inhibitors | RNA, Long Noncoding - metabolism | RNA | Pancreatic cancer | Physiological aspects | Genetic aspects | Research | Gene expression | Oncology | Cell cycle | Tumors
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7. Full Text Inhibition of c-Myc activity by ribosomal protein L11
by Sun, Xiao-Xin and Dai, Mu-Shui and Arnold, Hugh and Sears, Rosalie and Lu, Hua
The EMBO Journal, ISSN 0261-4189, 07/2007, Volume 26, Issue 14, pp. 3332 - 3345
The c‐Myc oncoprotein promotes cell growth by enhancing ribosomal biogenesis through upregulation of RNA polymerases I‐, II‐, and III‐dependent transcription.... 
ribosomal proteins | transcription | cell cycle | TRRAP | L11 | C‐Myc | C-Myc | Ribosomal proteins | Transcription | Cell cycle | MYC/MAX/MAD NETWORK | RNA-POLYMERASE-I | TRANSCRIPTIONAL ACTIVATION | c-Myc | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-SIZE | ONCOGENIC TRANSFORMATION | P53 | CELL BIOLOGY | ESSENTIAL COFACTOR | PATHWAY | GENES | DEGRADATION | Ribosomal Proteins - chemistry | RNA-Binding Proteins - genetics | Transcriptional Activation - genetics | Cell Proliferation | Humans | Phosphoproteins - metabolism | Promoter Regions, Genetic - genetics | Ribosomal Proteins - metabolism | S Phase | Serum | Transcription, Genetic | Acetylation | Protein Structure, Tertiary | Cell Line | Gene Expression | Ribosomal Proteins - genetics | Nuclear Proteins - metabolism | Phosphoproteins - genetics | Animals | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Protein Binding | Mice | Proto-Oncogene Proteins c-myc - genetics | Histones - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Proto-Oncogene Proteins c-myc - chemistry | RNA-Binding Proteins - metabolism | RNA, Small Interfering - metabolism | Proteins | Inhibitor drugs | Cellular biology | Molecular biology | Gene expression
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8. Full Text Direct Modulation of Small GTPase Activity and Function
by Cromm, Philipp M and Spiegel, Jochen and Grossmann, Tom N and Waldmann, Herbert
Angewandte Chemie International Edition, ISSN 1433-7851, 11/2015, Volume 54, Issue 46, pp. 13516 - 13537
Small GTPases are a family of GDP‐/GTP‐binding proteins that serve as biomolecular switches inside cells to control a variety of essential cellular processes.... 
inhibitors | cancer | drug design | proteins | small GTPases | ONCOGENIC K-RAS | GUANINE-NUCLEOTIDE-EXCHANGE | HUMAN CANCER-CELLS | TOXIN-CATALYZED GLUCOSYLATION | CHEMISTRY, MULTIDISCIPLINARY | IN-VITRO | SMALL-MOLECULE INHIBITORS | RHO FAMILY GTPASES | PROTEIN-PROTEIN INTERACTIONS | SPINAL-CORD-INJURY | RAS-EFFECTOR INTERACTIONS | Monomeric GTP-Binding Proteins - metabolism | Humans | Physiological aspects | Drug discovery | G proteins | Binding proteins | Gross domestic product | Protein binding | Proteins | Poverty | Drugs | Cellular | Modulation | Switches | Strategy | Holes | Modulators
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9. Full Text Ras Activity Levels Control the Development of Pancreatic Diseases
by Ji, Baoan and Tsou, Lilian and Wang, Huamin and Gaiser, Sebastian and Chang, David Z and Daniluk, Jaroslaw and Bi, Yan and Grote, Tobias and Longnecker, Daniel S and Logsdon, Craig D
Gastroenterology, ISSN 0016-5085, 2009, Volume 137, Issue 3, pp. 1072 - 1082.e6
Background & Aims Differentiated pancreatic acinar cells expressing endogenous levels of mutant K-Ras do not spontaneously develop pancreatic ductal... 
Gastroenterology and Hepatology | ACTIVATION | K-RAS | ONCOGENIC KRAS | MOUSE | ADULT MICE | INTRAEPITHELIAL NEOPLASIA | DUCTAL ADENOCARCINORNA | GASTROENTEROLOGY & HEPATOLOGY | CANCER | PROGRESSION | TRANSGENIC MICE | Pancreatic Neoplasms - metabolism | Humans | Pancreatic Neoplasms - pathology | Carcinoma, Pancreatic Ductal - metabolism | Mice, Transgenic | Pancreatic Neoplasms - genetics | Pancreatitis, Chronic - genetics | Carcinoma, Pancreatic Ductal - pathology | Carcinoma, Pancreatic Ductal - genetics | Pancreatitis, Chronic - pathology | Genes, ras - physiology | Animals | Cell Line, Tumor | Mice | Mutation | Pancreatitis, Chronic - metabolism | Genes, ras - genetics | Fluorescence | Development and progression | Transforming growth factors | Pancreatitis
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