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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
Journal Article
American journal of human genetics, ISSN 0002-9297, 2007, Volume 80, Issue 3, pp. 550 - 560
Journal Article
Cancer cell, ISSN 1535-6108, 2012, Volume 22, Issue 2, pp. 153 - 166
... ALL). The genetic alterations that activate kinase signaling in Ph-like ALL are poorly understood... 
GROWTH-FACTOR RECEPTOR | BCR-JAK2 FUSION GENE | ONCOLOGY | NUCLEAR-PORE | MYELOPROLIFERATIVE NEOPLASMS | ACUTE MYELOID-LEUKEMIA | OF-FUNCTION MUTATIONS | FLT3 MUTATIONS | CHILDHOOD | B-PROGENITOR | CHRONIC MYELOMONOCYTIC LEUKEMIA | CELL BIOLOGY | Recurrence | Humans | Molecular Sequence Data | RNA, Messenger - metabolism | Receptor, Platelet-Derived Growth Factor beta - genetics | Protein-Tyrosine Kinases - genetics | DNA Mutational Analysis | Base Sequence | Trans-Activators - genetics | Phosphorylation - drug effects | Philadelphia Chromosome | Receptors, Cytokine - genetics | Genetic Predisposition to Disease | RNA, Messenger - genetics | Risk Factors | Gene Expression Regulation, Leukemic - drug effects | Signal Transduction - genetics | Enzyme Activation - drug effects | Mutation - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | Animals | Signal Transduction - drug effects | Cell Transformation, Neoplastic | Oncogene Proteins, Fusion - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - enzymology | Mice | Protein Kinase Inhibitors - pharmacology | Gene Rearrangement - genetics | Sequence Deletion - genetics | Tyrosine | Platelet-derived growth factor | Cytokines | Genes | Oncology, Experimental | Genomes | Research | Gene expression | Population genetics | Hunger | Medical genetics | Genetic research | Nucleotide sequencing | Acute lymphocytic leukemia | Cancer | DNA sequencing
Journal Article
Journal Article
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
Cell (Cambridge), ISSN 0092-8674, 2016, Volume 167, Issue 1, pp. 233 - 247.e17
Journal Article