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Lancet, The, ISSN 0140-6736, 2012, Volume 380, Issue 9847, pp. 1059 - 1065
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2011, Volume 108, Issue 9, pp. 3761 - 3766
Journal Article
Nature Medicine, ISSN 1078-8956, 11/2016, Volume 22, Issue 11, pp. 1303 - 1313
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 06/2013, Volume 123, Issue 6, pp. 2551 - 2563
The PI3K signaling pathway regulates diverse cellular processes, including proliferation, survival, and metabolism, and is aberrantly activated in human... 
MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | GENE | PROTEIN-KINASE | DUAL PI3K/MTOR INHIBITOR | RIBOSOMAL S6 KINASE | FUNCTIONAL-CHARACTERIZATION | RSK4 | PHASE-I | EXPRESSION | RNAI SCREEN | Gene Expression Regulation, Enzymologic - drug effects | Apoptosis - drug effects | Heterocyclic Compounds, 3-Ring - pharmacology | Humans | Open Reading Frames | Transcriptome | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Quinolines - pharmacology | Breast Neoplasms - enzymology | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | MCF-7 Cells | Ribosomal Protein S6 Kinases, 90-kDa - antagonists & inhibitors | Female | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Cell Survival - drug effects | Gene Expression | Signal Transduction | Morpholines - pharmacology | Imidazoles - pharmacology | Breast Neoplasms - drug therapy | Drug Synergism | Xenograft Model Antitumor Assays | Animals | Tumor Burden - drug effects | Mice, Nude | Aminopyridines - pharmacology | Ribosomal Protein S6 Kinases, 90-kDa - genetics | Mice | Physiological aspects | Breast cancer | Genetic aspects | Cellular signal transduction | Research | Drug therapy | Drug resistance | Risk factors | Proteins | Medical research | Kinases | Tumors | Index Medicus | Abridged Index Medicus
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 Cell Biology, ISSN 1465-7392, 08/2018, Volume 20, Issue 8, pp. 954 - 965
BRCA1 deficiencies cause breast, ovarian, prostate and other cancers, and render tumours hypersensitive to poly(ADP-ribose) polymerase (PARP) inhibitors. To... 
PATHWAY CHOICE | STRAND BREAK REPAIR | RESECTION | DAMAGE-RESPONSE | 53BP1 | CLASS-SWITCH RECOMBINATION | FANCONI-ANEMIA | DIFFERENTIAL EXPRESSION ANALYSIS | POLYMERASE-ZETA | TELOMERES | CELL BIOLOGY | Osteosarcoma - drug therapy | Mad2 Proteins - metabolism | Humans | Multiprotein Complexes | Ovarian Neoplasms - pathology | Bone Neoplasms - pathology | DNA Breaks, Double-Stranded | Bone Neoplasms - metabolism | Breast Neoplasms - metabolism | Dose-Response Relationship, Drug | Ovarian Neoplasms - genetics | Telomere-Binding Proteins - genetics | DNA End-Joining Repair | HEK293 Cells | Female | Bone Neoplasms - genetics | Ovarian Neoplasms - metabolism | Bone Neoplasms - drug therapy | BRCA1 Protein - deficiency | Telomere-Binding Proteins - metabolism | Ovarian Neoplasms - drug therapy | Osteosarcoma - metabolism | Tumor Suppressor p53-Binding Protein 1 - metabolism | Recombinational DNA Repair | Tumor Suppressor p53-Binding Protein 1 - genetics | Cisplatin - pharmacology | Breast Neoplasms - drug therapy | Proteins - genetics | Xenograft Model Antitumor Assays | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Breast Neoplasms - genetics | Proteins - metabolism | Breast Neoplasms - pathology | Mad2 Proteins - genetics | Cell Line, Tumor | Mice | Osteosarcoma - genetics | Osteosarcoma - pathology | Care and treatment | DNA | Cancer cells | Breast cancer | Genetic aspects | Research | Gene expression | Single-stranded DNA | DNA damage | Homologous recombination | Poly(ADP-ribose) | Homology | Genomes | Inactivation | ADP | Proteins | Ribose | Null cells | Deoxyribonucleic acid--DNA | BRCA2 protein | CRISPR | Deactivation | BRCA1 protein | Poly(ADP-ribose) polymerase | Oligosaccharides | Double-strand break repair | Screens | Cisplatin | Polymerase | Inhibitors | Breast | Prostate | Viability | Tumors | Cancer | Index Medicus
Journal Article