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Cancer Cell, ISSN 1535-6108, 02/2014, Volume 25, Issue 2, pp. 243 - 256
Mutations in are prevalent in human cancers and universally predictive of resistance to anticancer therapeutics. Although it is widely accepted that... 
ACTIVATION | INHIBITION | ONCOGENIC RAS | TUMOR PROGRESSION | CHK1 | ONCOLOGY | INITIATION | COMBINATION | SUPPRESSION | ATR | KINASES | CELL BIOLOGY | Neoplasms - metabolism | Protein Kinases - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Humans | ras Proteins - metabolism | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | GTP Phosphohydrolases - antagonists & inhibitors | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Flow Cytometry | Neoplasms - genetics | DNA Damage - genetics | Female | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | DNA Damage - drug effects | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Membrane Proteins - genetics | Proto-Oncogene Proteins - genetics | Mutation - genetics | Animals | GTP Phosphohydrolases - metabolism | Membrane Proteins - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - metabolism | GTP Phosphohydrolases - genetics | Mice, Nude | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Checkpoint Kinase 1 | Mice | Cell Transformation, Neoplastic - pathology | Neoplasms - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Chemotherapy | DNA damage | DNA | Genetic research | DNA repair | Cancer | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 07/2011, Volume 475, Issue 7354, pp. 106 - 110
Reactive oxygen species (ROS) are mutagenic and may thereby promote cancer(1). Normally, ROS levels are tightly controlled by an inducible antioxidant program... 
TRANSFORMATION | OXIDATIVE STRESS | ACTIVATION | INHIBITION | K-RAS | PATHWAY | MULTIDISCIPLINARY SCIENCES | PANCREATIC-CANCER | HEME OXYGENASE-1 | MUTATIONS | EXPRESSION | NIH 3T3 Cells | Cell Proliferation | Pancreatic Neoplasms - metabolism | Reactive Oxygen Species - metabolism | Cytoskeletal Proteins - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Antioxidants - metabolism | Humans | JNK Mitogen-Activated Protein Kinases - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Cell Transformation, Neoplastic - genetics | Cytoskeletal Proteins - metabolism | NF-E2-Related Factor 2 - genetics | Intracellular Signaling Peptides and Proteins - genetics | Kelch-Like ECH-Associated Protein 1 | Proto-Oncogene Proteins B-raf - metabolism | Fibroblasts - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Oncogenes - genetics | Oxidation-Reduction | Pancreatic Neoplasms - pathology | Cells, Cultured | Pancreatic Neoplasms - genetics | NF-E2-Related Factor 2 - deficiency | Cell Transformation, Neoplastic - metabolism | Animals | Proto-Oncogene Proteins B-raf - genetics | Genes, myc - genetics | NF-E2-Related Factor 2 - metabolism | Adaptor Proteins, Signal Transducing - genetics | Alleles | Cell Line, Tumor | Mice | Adaptor Proteins, Signal Transducing - metabolism | Cell Transformation, Neoplastic - pathology | Polymerase chain reaction | Usage | Reactive oxygen species | Physiological aspects | Research | Gene expression | Oncogenes | Studies | Mass spectrometry | Rodents | Evacuations & rescues | Cancer | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 2017, Volume 292, Issue 31, pp. 12981 - 12993
H-Ras, K-Ras, and N-Ras are small GTPases that are important in the control of cell proliferation, differentiation, and survival, and their mutants occur... 
EVOLUTIONARY TREE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ESCHERICHIA-COLI | enzyme catalysis | Ras protein | allosteric regulation | conformational change | oncogene | enzyme structure | P21 | PHOSPHATE | STRUCTURAL BASIS | NUCLEOTIDE-FREE | ACTIVATING PROTEINS | EXPRESSION | GTP HYDROLYSIS | CONFORMATIONAL STATES | Proto-Oncogene Proteins p21(ras) - genetics | Allosteric Regulation | Humans | Crystallography, X-Ray | Guanosine Triphosphate - metabolism | Isoenzymes - chemistry | Dinucleoside Phosphates - chemistry | GTP Phosphohydrolases - chemistry | Isoenzymes - metabolism | Proto-Oncogene Proteins c-raf - chemistry | Proto-Oncogene Proteins p21(ras) - chemistry | Guanosine Triphosphate - chemistry | Membrane Proteins - metabolism | Protein Interaction Domains and Motifs | Peptide Fragments - genetics | Proto-Oncogene Proteins p21(ras) - metabolism | Recombinant Proteins - metabolism | Catalytic Domain | Peptide Fragments - metabolism | Biocatalysis | Proto-Oncogene Proteins c-raf - genetics | Isoenzymes - genetics | Membrane Proteins - genetics | Enzyme Stability | Guanosine Triphosphate - analogs & derivatives | Models, Molecular | Recombinant Proteins - chemistry | Dinucleoside Phosphates - metabolism | Proto-Oncogene Proteins c-raf - metabolism | Point Mutation | Peptide Fragments - chemistry | GTP Phosphohydrolases - metabolism | Membrane Proteins - chemistry | GTP Phosphohydrolases - genetics | Allosteric Site | Ligands | Protein Conformation | Amino Acid Substitution | Index Medicus | Enzymology
Journal Article
Molecular Systems Biology, ISSN 1744-4292, 2011, Volume 7, Issue 1, pp. 523 - n/a
Oncogenes such as K‐ ras mediate cellular and metabolic transformation during tumorigenesis. To analyze K‐Ras‐dependent metabolic alterations, we employed 13 C... 
cancer | metabolism | transcriptional analysis | metabolic flux analysis | Ras | MOUSE FIBROBLASTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIAL METABOLISM | TRANSFORMED FIBROBLASTS | LINES | P53 | FLUX ANALYSIS | DATABASE | AEROBIC GLYCOLYSIS | GENE-EXPRESSION | MUTATIONS | Neoplasms - metabolism | NIH 3T3 Cells | Cell Proliferation | Gas Chromatography-Mass Spectrometry | Oligonucleotide Array Sequence Analysis | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Gene Expression Regulation, Neoplastic | Glutamine - metabolism | Gene Expression Profiling | Flow Cytometry | Neoplasms - genetics | Cell Transformation, Neoplastic - genetics | Isotope Labeling | Fibroblasts - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Cell Transformation, Neoplastic - metabolism | Citric Acid Cycle | Animals | Cell Line, Tumor | Glucose - metabolism | Glycolysis | Fibroblasts - cytology | Mice | Neoplasms - pathology | Cell Line, Transformed | Tricarboxylic acid cycle | Transformation | Profiling | Downstream effects | Oxidative metabolism | Glucose | Proteins | Mitochondria | Alterations | Stable isotopes | Fluctuations | Metabolism | Gene expression | Organic chemistry | Computer applications | Transformations | Tracers | System effectiveness | Biotechnology | Reactive oxygen species | Transcription | Change detection | Genes | Amino acids | Intracellular signalling | Pyruvic acid | Biosynthesis | Myc protein | Kinases | Glucose metabolism | Metabolic flux | Metabolites | Carbon 13 | Adenine | Tumor cell lines | Fluxes | Nutrient uptake | Nitrogen | Carbon | Intermediates | Carbon cycle | Decoupling | Cell lines | Intracellular | Lactic acid | Apoptosis | Glutamine | Cancer | Index Medicus
Journal Article
Journal Article
Nature, ISSN 0028-0836, 04/2013, Volume 496, Issue 7443, pp. 101 - 105
Journal Article
Cancer Cell, ISSN 1535-6108, 09/2012, Volume 22, Issue 3, pp. 304 - 317
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 04/2012, Volume 18, Issue 8, pp. 2316 - 2325
Purpose: This study evaluated the clinical relevance of the dual-targeting strategy involving PI3K/AKT/mTOR and RAF/MEK/ERK pathways. Experimental Design: We... 
COLON-CANCER | METASTATIC MELANOMA | PIK3CA MUTATIONS | PI3K | ONCOLOGY | COLORECTAL-CANCER | RESISTANCE | BRAF | ANTITUMOR-ACTIVITY | MEK INHIBITORS | TUMORS | Neoplasms - metabolism | Extracellular Signal-Regulated MAP Kinases - drug effects | TOR Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Middle Aged | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | Young Adult | MAP Kinase Signaling System - genetics | TOR Serine-Threonine Kinases - genetics | Neoplasms - genetics | Aged, 80 and over | Adult | Female | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Adolescent | Aged | Mutation | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
FEBS Journal, ISSN 1742-464X, 12/2015, Volume 282, Issue 24, pp. 4810 - 4821
Journal Article