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Cancer Research, ISSN 0008-5472, 02/2018, Volume 78, Issue 4 Supplement, pp. BS3-1 - BS3-1
Journal Article
Nature Genetics, ISSN 1061-4036, 12/2013, Volume 45, Issue 12, pp. 1439 - 1445
Journal Article
JOURNAL OF CLINICAL ONCOLOGY, ISSN 0732-183X, 05/2019, Volume 37, Issue 14, pp. 1148 - 1148
Journal Article
Journal Article
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
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
The Mailer Review, ISSN 1936-4679, 09/2016, Volume 10, Issue 1, p. 1
Journal Article
The Mailer Review, ISSN 1936-4679, 09/2016, Volume 10, Issue 1, p. 337
Journal Article
British Journal of Cancer, ISSN 0007-0920, 03/2017, Volume 116, Issue 6, pp. 726 - 730
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
Cancer Discovery, ISSN 2159-8274, 03/2019, Volume 9, Issue 3, pp. 323 - 325
Standard treatment for estrogen receptor-positive metastatic breast cancer involves antiestrogen therapy used alone or in combination with inhibitors of CDK4/6... 
ONCOLOGY | BCL2
Journal Article
Journal Article