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Molecular Oncology, ISSN 1574-7891, 08/2013, Volume 7, Issue 4, pp. 776 - 790
Targeted therapy development in head and neck squamous cell carcinoma (HNSCC) is challenging given the rarity of activating mutations. Additionally, HNSCC... 
Head and neck cancer | Human papillomavirus | NOTCH1 | PI3K | EGFR | Xenografts | HEAD | PLUS CETUXIMAB | PHASE-II | HUMAN-PAPILLOMAVIRUS | GENE | ONCOLOGY | GROWTH | NECK | MUTATIONS | CARCINOMA | REVEALS | Gonanes - pharmacology | Immunohistochemistry | Antibodies, Monoclonal, Humanized - therapeutic use | ErbB Receptors - metabolism | Head and Neck Neoplasms - virology | Carcinoma, Squamous Cell - virology | Humans | Computational Biology | ErbB Receptors - genetics | Head and Neck Neoplasms - drug therapy | Receptor, Notch2 - metabolism | Receptor, Notch2 - genetics | Phosphatidylinositol 3-Kinases - metabolism | Receptor, Notch1 - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Blotting, Western | Xenograft Model Antitumor Assays | Alphapapillomavirus - pathogenicity | Squamous Cell Carcinoma of Head and Neck | Animals | Carcinoma, Squamous Cell - drug therapy | Mice | Cetuximab | Receptor, Notch1 - genetics | Drugs and athletes | Medical colleges | Squamous cell carcinoma | Care and treatment | Genes | Disease susceptibility | Gene expression | Drug approval | Nuclear radiation | Analysis | Tumor proteins | Papillomavirus infections | Cancer | Hypothesis testing | Epidermal growth factor receptors | p53 Protein | AKT protein | Patients | Epidemiology | 1-Phosphatidylinositol 3-kinase | Antitumor agents | Mutation | Tumors | Papers | Paper
Journal Article
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 2017, Volume 109, Issue 1, p. djw189
Background: We have an incomplete understanding of the differences between cancer stem cells (CSCs) in human papillomavirus-positive (HPV-positive) and... 
UNITED-STATES | TO-MESENCHYMAL TRANSITION | METASTASIS | ONCOLOGY | SIGNALING PATHWAY | RESISTANCE | HUMAN-PAPILLOMAVIRUS | INHIBITORS | MUTATIONS | CARCINOMA | EXPRESSION | Neoplasm Transplantation | Cell Proliferation | Head and Neck Neoplasms - virology | Cadherins - metabolism | TOR Serine-Threonine Kinases - metabolism | Neoplastic Stem Cells - drug effects | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - virology | Humans | Transcriptome | RNA, Messenger - analysis | Head and Neck Neoplasms - metabolism | SOXB1 Transcription Factors - metabolism | Neoplastic Stem Cells - metabolism | SOXB1 Transcription Factors - genetics | Cell Division | Hyaluronan Receptors - metabolism | Neoplastic Stem Cells - pathology | Female | Antineoplastic Agents - pharmacology | Tumor Cells, Cultured | Spheroids, Cellular | Aldehyde Dehydrogenase - metabolism | Phosphatidylinositol 3-Kinase - metabolism | ErbB Receptors - metabolism | Signal Transduction | Head and Neck Neoplasms - drug therapy | Papillomaviridae - isolation & purification | Animals | Carcinoma, Squamous Cell - drug therapy | Sequence Analysis, RNA | Phosphatidylinositol 3-Kinase - genetics | Mice, Nude | Head and Neck Neoplasms - genetics | Mice | Cell Transformation, Neoplastic - drug effects | Antigens, CD
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2014, Volume 9, Issue 11, p. e113037
Background: The activation of the MAPK and PI3K/AKT/mTOR pathways is implicated in the majority of cancers. Activating mutations in both of these pathways has... 
BREAST-CANCER | CARCINOMA-CELLS | COLON-CANCER | SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | ORAL MEK INHIBITOR | SMALL-CELL LUNG | TUBEROUS SCLEROSIS | ANTITUMOR-ACTIVITY | PHASE-I | PREVIOUSLY TREATED PATIENTS | Diphenylamine - pharmacology | TOR Serine-Threonine Kinases - metabolism | Humans | Immunoblotting | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | TOR Serine-Threonine Kinases - antagonists & inhibitors | Diphenylamine - analogs & derivatives | Colorectal Neoplasms - drug therapy | Female | Benzamides - pharmacology | Colorectal Neoplasms - metabolism | Antineoplastic Combined Chemotherapy Protocols | Drug Synergism | Xenograft Model Antitumor Assays | Animals | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Colorectal Neoplasms - pathology | Mitogen-Activated Protein Kinases - metabolism | Models | Health aspects | Analysis | Colorectal cancer | TOR protein | Cell culture | Biotechnology | Downstream effects | Colorectal carcinoma | Clinical trials | Oncology | AKT protein | Kinases | K-Ras protein | Cell growth | Pathways | Xenografts | Drug dosages | Pharmaceutical sciences | Extracellular signal-regulated kinase | MAP kinase | Pharmacology | Tumor cell lines | Patients | 1-Phosphatidylinositol 3-kinase | Medicine | Inhibitors | Cell lines | Certificates of need | Mutation | Cancer | Apoptosis | Tumors
Journal Article
BMC Cancer, ISSN 1471-2407, 02/2018, Volume 18, Issue 1, pp. 136 - 12
Background: Polo-like kinase 1 (Plk1) is a serine/threonine kinase that is a key regulator of multiple stages of mitotic progression. Plk1 is upregulated in... 
TAK-960 | Plk1 | Colorectal cancer | Patient-derived xenograft | POLY(ADP-RIBOSE) POLYMERASE | APOPTOSIS | SOLID TUMORS | TUMOR SUPPRESSION | CELL-CYCLE ARREST | PLK1 INHIBITION | DRUG TARGETS | MEK INHIBITOR | ONCOLOGY | DNA-DAMAGE-RESPONSE | PHASE-I | Chemotherapy | Usage | Prognosis | Development and progression | Research | Biological markers | Cancer
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 02/2012, Volume 18, Issue 4, pp. 1051 - 1062
Journal Article
Molecular Cancer Therapeutics, ISSN 1535-7163, 12/2010, Volume 9, Issue 12, pp. 3351 - 3362
Journal Article
Frontiers in Pharmacology, ISSN 1663-9812, 2015, Volume 6, Issue MAY, p. 120
Aurora A kinase and MEK inhibitors induce different, and potentially complementary, effects on the cell cycle of malignant cells, suggesting a rational basis... 
Human tumor xenografts | KRAS mutation | MEK | Aurora A kinase | Alisertib | PIK3CA | Colorectal cancer | Trametinib | colorectal cancer | ADVANCED SOLID TUMORS | ALISERTIB MLN8237 | PHOSPHORYLATION | human tumor xenografts | P53 | trametinib | CETUXIMAB | MELANOMA | THERAPY | alisertib | RAS MUTATIONS | SELUMETINIB | PHARMACOLOGY & PHARMACY | PHASE-I
Journal Article