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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
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 5, pp. 575 - 586
Prostate cancer is characterized by its dependence on androgen receptor (AR) and frequent activation of PI3K signaling. We find that AR transcriptional output... 
TARGET | CELLS | ONCOLOGY | PATHWAY | DUAL PI3K/MTOR INHIBITOR | KINASE | TUMOR-SUPPRESSOR | AKT | INDUCTION | MTOR COMPLEX | HORMONAL-THERAPY | CELL BIOLOGY | Receptor, ErbB-3 - metabolism | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Phosphoprotein Phosphatases - metabolism | Receptors, Androgen - metabolism | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Male | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Prostatic Neoplasms - genetics | Receptors, Androgen - drug effects | Transfection | RNA Interference | Time Factors | Transcription, Genetic | Receptor, ErbB-2 - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Genes, Reporter | Prostatic Neoplasms - drug therapy | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | PTEN Phosphohydrolase - deficiency | Androgen Antagonists - pharmacology | Receptor, ErbB-3 - antagonists & inhibitors | Mice, Transgenic | Nuclear Proteins - metabolism | Mice, SCID | Proto-Oncogene Proteins c-myc - metabolism | Mice, Knockout | Xenograft Model Antitumor Assays | Magnetic Resonance Imaging | Feedback, Physiological | Animals | Signal Transduction - drug effects | Tumor Burden - drug effects | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-myc - genetics | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Phosphatases | Health aspects | Phosphotransferases | Prostate cancer | Analysis | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 06/2012, Volume 486, Issue 7403, pp. 405 - 409
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
Clinical Cancer Research, ISSN 1078-0432, 05/2012, Volume 18, Issue 9, pp. 2502 - 2514
Purpose: The clinical use of BRAF inhibitors is being hampered by the acquisition of drug resistance. This study shows the potential therapeutic use of the... 
BREAST-CANCER | MULTIPLE-MYELOMA | APOPTOSIS | PHASE-II TRIAL | TANESPIMYCIN 17-AAG | TRASTUZUMAB | ONCOLOGY | BIM | ACQUIRED-RESISTANCE | MELANOMA-CELLS | POTENTIAL MECHANISM | Prospective Studies | Apoptosis - drug effects | Humans | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Immunoenzyme Techniques | Forkhead Transcription Factors - metabolism | Colony-Forming Units Assay | Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization | Phthalic Acids - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Real-Time Polymerase Chain Reaction | Proto-Oncogene Proteins B-raf - metabolism | Membrane Proteins - genetics | Melanoma - pathology | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Apoptosis Regulatory Proteins - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Indoles - adverse effects | Membrane Proteins - antagonists & inhibitors | Signal Transduction - drug effects | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Cell Line, Tumor | HSP90 Heat-Shock Proteins - metabolism | Mice | Mice, Inbred BALB C | Forkhead Box Protein O3 | Azabicyclo Compounds - pharmacology | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | Flow Cytometry | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | Forkhead Transcription Factors - antagonists & inhibitors | Melanoma - metabolism | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | RNA, Messenger - genetics | Proto-Oncogene Proteins - genetics | Forkhead Transcription Factors - genetics | Phosphatidylinositol 3-Kinases - genetics | Animals | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Myeloid Cell Leukemia Sequence 1 Protein | Apoptosis Regulatory Proteins - antagonists & inhibitors | Fluorescent Antibody Technique | Sulfonamides - adverse effects | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-bcl-2 - genetics | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Index Medicus
Journal Article
Journal Article
CLINICAL CANCER RESEARCH, ISSN 1078-0432, 09/2015, Volume 21, Issue 17, pp. 4014 - 4021
Journal Article
Journal Article
Journal Article
Cancer Research, ISSN 0008-5472, 08/2011, Volume 71, Issue 15, pp. 5067 - 5074
(V600E)B-RAF mutation is found in 50% to 60% of melanomas, and the novel agents PLX4032/vemurafenib and GSK2118436 that inhibit the (V600E)B-RAF kinase achieve... 
Apoptosis - drug effects | Humans | Multiprotein Complexes | Neoplasm Proteins - physiology | Recombinant Fusion Proteins - physiology | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Receptor, Platelet-Derived Growth Factor beta - genetics | Quinolines - pharmacology | Mechanistic Target of Rapamycin Complex 1 | Receptor, Platelet-Derived Growth Factor beta - antagonists & inhibitors | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Spheroids, Cellular - drug effects | MAP Kinase Kinase Kinases - antagonists & inhibitors | Proteins - physiology | Transcription Factors - physiology | Receptor, Platelet-Derived Growth Factor beta - physiology | Morpholines - pharmacology | Transcription Factors - antagonists & inhibitors | Imidazoles - pharmacology | Proto-Oncogene Proteins c-akt - physiology | Melanoma - pathology | Sulfonamides - pharmacology | Drug Synergism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Point Mutation | Vemurafenib | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Phosphatidylinositol 3-Kinases - physiology | Signal Transduction - physiology | TOR Serine-Threonine Kinases | Drug Resistance, Neoplasm - physiology | Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Drug Screening Assays, Antitumor | Index Medicus | vemurafenib | targeted therapy | melanoma | AKT | B-RAF | acquired resistance
Journal Article
Journal Article
Cancer Cell, ISSN 1535-6108, 07/2014, Volume 26, Issue 1, pp. 136 - 149
Activation of the phosphoinositide 3-kinase (PI3K) pathway occurs frequently in breast cancer. However, clinical results of single-agent PI3K inhibitors have... 
DRUG | INACTIVATION | ADVANCED SOLID TUMORS | MAMMARY-TUMORS | GENE | ONCOLOGY | PATHWAY INHIBITORS | CYCLIN D1 EXPRESSION | GROWTH | PHASE-I | PRECLINICAL EVALUATION | CELL BIOLOGY | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Phosphorylation | Phosphatidylinositol Phosphates - metabolism | Cyclin-Dependent Kinase 4 - genetics | Humans | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Dose-Response Relationship, Drug | Breast Neoplasms - enzymology | Transfection | MCF-7 Cells | RNA Interference | Time Factors | Female | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - metabolism | Cell Survival - drug effects | Genetic Predisposition to Disease | Retinoblastoma Protein - metabolism | Cyclin-Dependent Kinase 6 - genetics | Treatment Outcome | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Mice, SCID | Breast Neoplasms - drug therapy | Drug Synergism | Phosphatidylinositol 3-Kinases - genetics | Xenograft Model Antitumor Assays | Protein Kinase Inhibitors - administration & dosage | Phenotype | Animals | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Signal Transduction - drug effects | Breast Neoplasms - pathology | Mice, Nude | Cell Proliferation - drug effects | Mice | Mutation | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Medical colleges | Breast cancer | Index Medicus
Journal Article