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Clin Cancer Res 2008, 14:342–346.PubMedCrossRef 53. Roberts PJ, Der CJ: Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer. Oncogene 2007, 26:3291–3310.PubMedCrossRef 54. Mhaidat click here NM, Zhang XD, Jiang CC, Hersey P: Selleck Volasertib Docetaxel-induced apoptosis of human melanoma is mediated by activation of c-Jun NH2-terminal kinase and inhibited by the mitogen-activated protein kinase extracellular signal-regulated kinase 1/2 pathway. Clin Cancer Res 2007, 13:1308–1314.PubMedCrossRef 55. Yu C, Wang S, Dent P, Grant S: Sequence-dependent potentiation of paclitaxel-mediated apoptosis in human leukemia cells by inhibitors of the mitogen-activated protein

kinase kinase/mitogen-activated protein kinase pathway. Mol Pharmacol 2001, 60:143–154.PubMed 56. Wang S, Guo CY, Castillo A, Dent P, Grant S: Effect of bryostatin 1 on taxol-induced apoptosis and cytotoxicity in human leukemia cells (U937). Biochem Pharmacol 1998, 56:635–644.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions HYN participated in research design, the writing of the paper, the performance of the research and data analysis. JHW

participated in the performance of the research and data analysis. HL participated in the performance of the research. PH participated in research design and data analysis. All authors read and approved the final manuscript.”
“Background Lung cancer is the leading cause Selumetinib cost of death world wide. The non-small cell lung cancer (NSCLC) accounts for 75-85% among all lung cancers. The conventional treatment e.g. surgery, radiotherapy and chemotherapy yields a dismal overall 5-year survival of 14% which necessitates the development of new treatment options [1]. With advances in cytogenetic and molecular biology, the detection and analysis of tumor suppressor gene and oncogene may provide

predictive values for prognosis and treatment choice for NSCLC. Among these molecular markers, the epidermal growth factor receptor (EGFR) and cyclooxygenase-2 see more (COX-2) over expression are common in NSCLC [2–9]. EGFR (HER1, ErbB) is a transmembrane glycoprotein with three functional domains: an extracellular domain containing two EGF binding sites; a hydrophobic transmembrane domain and a cytoplasmic domain (tyrosine kinase (TK) and a carboxyl autophosphorylation region) [10, 11]. EGFR is abnormally upregulated and activated in a variety of tumors [12]. Deregulation of receptor tyrosine kinases as a result of overexpression or activating mutations leads to the promotion of cell proliferation or migration, inhibition of cell death, or the induction of angiogenesis [13, 14]. The expression and activity of EGFR are determinants of response to target therapy and radiosensitivity in several tumour types [15].

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