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Nature (London), ISSN 1476-4687, 2016, Volume 534, Issue 7605, pp. 55 - 62
Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly understood... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors
Journal Article
1997, Cancer surveys, ISBN 0879695188, Volume 29., vi, 363
Book
Cancer cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, Lkb1 deletion and activation of Kras G12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these... 
CELLCYCLE | SIGNALING | INACTIVATION | SUPPRESSOR | SIGNATURES | ONCOLOGY | SRC | ADENOCARCINOMA | SENSITIVITY | MUTATIONS | LKB1/STK11 | EXPRESSION | TUMORIGENESIS | CELL BIOLOGY | Lung Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - deficiency | Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Genomics | Humans | Lung Neoplasms - metabolism | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - genetics | Phosphorylation - genetics | RNA Interference | Gene Expression Regulation, Neoplastic - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - metabolism | Signal Transduction - genetics | Enzyme Inhibitors - therapeutic use | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Focal Adhesion Protein-Tyrosine Kinases - genetics | Focal Adhesions - genetics | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | src-Family Kinases - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | ras Proteins - genetics | Lung Neoplasms - pathology | Cell Transdifferentiation - genetics | Protein-Tyrosine Kinases - genetics | Neoplasm Metastasis - drug therapy | Mice, Mutant Strains | Protein-Serine-Threonine Kinases - antagonists & inhibitors | src-Family Kinases - metabolism | Female | Drug Therapy, Combination | Lung Neoplasms - genetics | Cell Adhesion - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | src-Family Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | Xenograft Model Antitumor Assays | Neoplasm Metastasis - genetics | Animals | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Focal Adhesions - metabolism | Proteomics | Protein Kinase Inhibitors - pharmacology | Oncology, Experimental | Analysis | Lung cancer | Development and progression | Metastasis | Research | Cancer
Journal Article
Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 1897 - 17
The cellular decision regarding whether to undergo proliferation or death is made at the restriction (R)-point, which is disrupted in nearly all tumors. The... 
UBIQUITINATION | AML1-ETO | ACETYLATION | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | PROTEINS | QUANTITATIVE-ANALYSIS | POLYCOMB | CANCER | KINASES | FAMILY | Chromatin - metabolism | RNA, Small Interfering - genetics | Myeloid-Lymphoid Leukemia Protein - metabolism | TOR Serine-Threonine Kinases - metabolism | Core Binding Factor Alpha 3 Subunit - antagonists & inhibitors | Humans | Polycomb-Group Proteins - metabolism | TOR Serine-Threonine Kinases - genetics | Cell Cycle Checkpoints - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Chromatin - chemistry | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Signal Transduction | Epithelial Cells - pathology | MAP Kinase Kinase 1 - metabolism | Imidazoles - pharmacology | Cyclin-Dependent Kinase 4 - metabolism | Piperazines - pharmacology | Cell Cycle Checkpoints - drug effects | Polycomb-Group Proteins - genetics | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Line, Tumor | MAP Kinase Kinase 4 - genetics | RNA, Small Interfering - metabolism | ras Proteins - genetics | Core Binding Factor Alpha 3 Subunit - metabolism | Epithelial Cells - metabolism | Nitriles - pharmacology | Cyclin-Dependent Kinase 4 - genetics | Epithelial Cells - drug effects | ras Proteins - metabolism | Drosophila melanogaster - genetics | Chromatin Assembly and Disassembly - drug effects | Drosophila melanogaster - metabolism | MAP Kinase Kinase 1 - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | MAP Kinase Kinase 4 - metabolism | HEK293 Cells | MAP Kinase Kinase 4 - antagonists & inhibitors | Chromatin - drug effects | Histone-Lysine N-Methyltransferase - genetics | Drosophila melanogaster - cytology | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Sirolimus - pharmacology | Animals | Histone-Lysine N-Methyltransferase - metabolism | Myeloid-Lymphoid Leukemia Protein - genetics | Core Binding Factor Alpha 3 Subunit - genetics | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Polycomb group proteins | Regulators | Molecular modelling | S phase | Genes | Cell cycle | Loci | Runx3 protein | Recruitment | Tumors | Chromatin remodeling
Journal Article
PLoS genetics, ISSN 1553-7404, 2012, Volume 8, Issue 7, p. e1002816
Journal Article
Leukemia, ISSN 1476-5551, 2011, Volume 25, Issue 7, pp. 1080 - 1094
The Ras/Raf/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK... 
targeted therapy | Ras | therapeutic sensitivity | Raf | resistance | ERK | ABROGATE CYTOKINE DEPENDENCY | INITIATION-FACTOR 4E | ACUTE MYELOID-LEUKEMIA | KINASE INHIBITOR PROTEIN | DRUG-INDUCED APOPTOSIS | BONE-MARROW MICROENVIRONMENT | ONCOLOGY | ACUTE LYMPHOBLASTIC-LEUKEMIA | CHRONIC LYMPHOCYTIC-LEUKEMIA | MURINE HEMATOPOIETIC-CELLS | HEMATOLOGY | SIGNAL-REGULATED KINASE | ras Proteins - genetics | MAP Kinase Signaling System - physiology | Mitogen-Activated Protein Kinase Kinases - genetics | Apoptosis - drug effects | raf Kinases - antagonists & inhibitors | Humans | Neoplasm Proteins - physiology | Mitogen-Activated Protein Kinase Kinases - physiology | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - genetics | Gene Expression Regulation, Leukemic - genetics | raf Kinases - physiology | MAP Kinase Signaling System - genetics | Drug Design | Antineoplastic Agents - pharmacology | Extracellular Signal-Regulated MAP Kinases - physiology | Neoplasm Proteins - genetics | raf Kinases - genetics | ras Proteins - physiology | Cell Division - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | ras Proteins - antagonists & inhibitors | Gene Expression Regulation, Leukemic - drug effects | Leukemia - drug therapy | Cell Division - drug effects | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | MAP Kinase Signaling System - drug effects | Models, Biological | Phosphatidylinositol 3-Kinases - physiology | Apoptosis - physiology | Drug Resistance, Neoplasm - physiology | Drug Resistance, Neoplasm - drug effects | Chemotherapy | Extracellular signal-regulated kinases | Leukemia | Physiological aspects | Genetic aspects | Research | Drug therapy | Health aspects | Mitogen-activated protein kinases | Cancer
Journal Article
Nature genetics, ISSN 1546-1718, 2015, Volume 47, Issue 3, pp. 250 - 256
... not all patients with BRAF gene mutation and are largely ineffective in those with RAS gene mutation because of resistance(5-14). Through a genetic screen in BRAF-mutant tumor cells, we show that the Hippo pathway effector YAP... 
COLON-CANCER | SURVIVAL | LUNG | ACTIVATION | INHIBITION | MELANOMA | SIGNALING PATHWAY | TRANSCRIPTION | GENETICS & HEREDITY | BRAF | KRAS | Humans | Molecular Targeted Therapy | Phosphoproteins - metabolism | Gene Knockdown Techniques | Heterografts | MAP Kinase Signaling System - genetics | HEK293 Cells | Female | MAP Kinase Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins B-raf - metabolism | MAP Kinase Kinase Kinases - genetics | Protein-Serine-Threonine Kinases - genetics | MAP Kinase Kinase Kinases - metabolism | Phosphoproteins - genetics | Mice, SCID | HT29 Cells | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Animals | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Mice, Inbred NOD | Biomarkers, Tumor - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Transcription Factors | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Genes, ras | Antimitotic agents | Gene mutations | Genetic aspects | Research | Antineoplastic agents | Drug resistance | Health aspects | Thyroid cancer | Lung cancer | Colorectal cancer | Melanoma | Kinases | Charitable foundations | Cancer therapies | Design of experiments | Tumors
Journal Article
PLoS genetics, ISSN 1553-7404, 2014, Volume 10, Issue 11, p. e1004783
Journal Article