Activity of the MEK inhibitor selumetinib (AZD6244; ARRY-142886) in nasopharyngeal cancer cell lines
暂无分享,去创建一个
S. Tsui | P. Ng | E. Hui | B. Ma | M. Ng | A. Chan | Vivian W Y Lui | S. W. Tsao | C. Lau | S. Cheng | C. S. Cheung | K. Ho | V. Lui | Kakiu Ho
[1] S. Tsao,et al. Preclinical evaluation of the AKT inhibitor MK-2206 in nasopharyngeal carcinoma cell lines , 2013, Investigational New Drugs.
[2] W. Liao,et al. The Ras signaling pathway mediates cetuximab resistance in nasopharyngeal carcinoma. , 2011, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.
[3] J. Minna,et al. STAT3 mediates resistance to MEK inhibitor through microRNA miR-17. , 2011, Cancer research.
[4] H. Hong,et al. Acquisition of chemoresistance in intrahepatic cholangiocarcinoma cells by activation of AKT and extracellular signal-regulated kinase (ERK)1/2. , 2011, Biochemical and biophysical research communications.
[5] Kang-Yell Choi,et al. MEK1/2 inhibitors AS703026 and AZD6244 may be potential therapies for KRAS mutated colorectal cancer that is resistant to EGFR monoclonal antibody therapy. , 2011, Cancer research.
[6] A. Iafrate,et al. BRAF Gene Amplification Can Promote Acquired Resistance to MEK Inhibitors in Cancer Cells Harboring the BRAF V600E Mutation , 2010, Science Signaling.
[7] W. Sellers,et al. PIK3CA mutation uncouples tumor growth and cyclin D1 regulation from MEK/ERK and mutant KRAS signaling. , 2010, Cancer research.
[8] S. Tsao,et al. Abstract 1638: Preclinical evaluation of the PI3K inhibitor BEZ235 in nasopharyngeal carcinoma cell lines , 2010 .
[9] S. Cook,et al. Intrinsic resistance to the MEK1/2 inhibitor AZD6244 (ARRY‐142886) is associated with weak ERK1/2 signalling and/or strong PI3K signalling in colorectal cancer cell lines , 2009, International journal of cancer.
[10] Y. Bang,et al. Combination of EGFR and MEK1/2 inhibitor shows synergistic effects by suppressing EGFR/HER3-dependent AKT activation in human gastric cancer cells , 2009, Molecular Cancer Therapeutics.
[11] P. Pandolfi,et al. Inhibition of mTORC1 leads to MAPK pathway activation through a PI3K-dependent feedback loop in human cancer. , 2008, The Journal of clinical investigation.
[12] T. Mok,et al. A phase II study of patients with metastatic or locoregionally recurrent nasopharyngeal carcinoma and evaluation of plasma Epstein–Barr virus DNA as a biomarker of efficacy , 2008, Cancer Chemotherapy and Pharmacology.
[13] Mhairi A. Morris,et al. Epstein-Barr Virus-Encoded LMP1 Regulates Epithelial Cell Motility and Invasion via the ERK-MAPK Pathway , 2008, Journal of Virology.
[14] M. Herlyn,et al. The Mitogen-Activated Protein/Extracellular Signal-Regulated Kinase Kinase Inhibitor AZD6244 (ARRY-142886) Induces Growth Arrest in Melanoma Cells and Tumor Regression When Combined with Docetaxel , 2008, Clinical Cancer Research.
[15] Gen Sheng Wu,et al. ERK-dependent MKP-1-mediated cisplatin resistance in human ovarian cancer cells. , 2007, Cancer research.
[16] H. Huynh,et al. AZD6244 and doxorubicin induce growth suppression and apoptosis in mouse models of hepatocellular carcinoma , 2007, Molecular Cancer Therapeutics.
[17] Paul D. Martin,et al. AZD6244 (ARRY-142886), a potent inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 kinases: mechanism of action in vivo, pharmacokinetic/pharmacodynamic relationship, and potential for combination in preclinical models , 2007, Molecular Cancer Therapeutics.
[18] N. Raab-Traub,et al. Unique Signaling Properties of CTAR1 in LMP1-Mediated Transformation , 2007, Journal of Virology.
[19] M. Osmak,et al. Activation of mitogen-activated protein kinases by cisplatin and their role in cisplatin-resistance. , 2007, Cancer letters.
[20] Vivienne Marsh,et al. Biological Characterization of ARRY-142886 (AZD6244), a Potent, Highly Selective Mitogen-Activated Protein Kinase Kinase 1/2 Inhibitor , 2007, Clinical Cancer Research.
[21] Ting-Chao Chou,et al. Theoretical Basis, Experimental Design, and Computerized Simulation of Synergism and Antagonism in Drug Combination Studies , 2006, Pharmacological Reviews.
[22] Y. Lau,et al. Epstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cells. , 2006, Neoplasia.
[23] A. Hui,et al. PIK3CA mutations in nasopharyngeal carcinoma , 2006, International journal of cancer.
[24] Todd R. Golub,et al. BRAF mutation predicts sensitivity to MEK inhibition , 2006, Nature.
[25] M. Beeram,et al. Raf: a strategic target for therapeutic development against cancer. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[26] M. Beeram,et al. Regulation of c-Raf-1: therapeutic implications. , 2003, Clinical advances in hematology & oncology : H&O.
[27] Y. Wong,et al. Alterations of Biologic Properties and Gene Expression in Nasopharyngeal Epithelial Cells by the Epstein-Barr Virus–Encoded Latent Membrane Protein 1 , 2003, Laboratory Investigation.
[28] S. Tsao,et al. The significance of LMP1 expression in nasopharyngeal carcinoma. , 2002, Seminars in cancer biology.
[29] A. Hui,et al. Genome wide detection of oncogene amplifications in nasopharyngeal carcinoma by array based comparative genomic hybridization. , 2002, International journal of oncology.
[30] N. Cooper,et al. Activation of a ras-MAPK-dependent pathway by Epstein-Barr virus latent membrane protein 1 is essential for cellular transformation. , 1998, Virology.
[31] Q. Tao,et al. Preclinical activity of gefitinib in non-keratinizing nasopharyngeal carcinoma cell lines and biomarkers of response , 2010, Investigational new drugs.
[32] C. Tzen,et al. PIK3CA mutation occurs in nasopharyngeal carcinoma but does not significantly influence the disease-specific survival , 2009, Medical oncology.
[33] S. Thibodeau,et al. Signal-Regulated Kinase and Raf Proteins Negative Feedback Pathways between Extracellular BRAF V 600 E Disrupts AZD 6244-Induced Abrogation of Updated , 2008 .
[34] T. Poon,et al. Antitumor effect and enhancement of cytotoxic drug activity by cetuximab in nasopharyngeal carcinoma cells. , 2005, In vivo.