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The Effects and Mechanism on the Proliferation of Human Adenocarcinoma Cell SPC-A1 of Gefitinib Combined with Docetaxel in Different Administration.

Author: ZhangWenYing
Tutor: ZhangWeiMin
School: Guangzhou Medical College
Course: Oncology
Keywords: Human lung adenocarcinoma cells SPC-A1 Docetaxel Gefitinib Cell growth Signaling proteins Phosphorylation
CLC: R734.2
Type: Master's thesis
Year: 2011
Downloads: 11
Quote: 0
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Background and Purpose chemotherapy with epidermal growth factor receptor tyrosine kinase inhibitor combination treatment of advanced non- small cell lung cancer (epidermal growth factor receptor-tyrosine kinase inhibitors, EGFR-TKIs) to create synergies administration timing . Previous studies have shown that both at the same time and the first gefitinib Nepal after chemotherapy interaction with the cell cycle is closely related to , but chemotherapy sequential gefitinib Nepal synergies mechanism , remains unclear . In this study, through the concept of docetaxel and gefitinib Niger different timing application on the growth of human lung adenocarcinoma SPC-A1 cells and EGFR signaling protein ERK , AKT and insulin-like growth factor ( insulin - like growth factor IGF ) 1 receptor (IGF-1R) expression and phosphorylation of the role , to explore the efficiency of both sequential medication may cytological mechanisms . Method qPCR-HRM assay cells EGFR and K-ras gene mutation ; MTT chromogenic spectrophotometric detection of cell proliferation ; by Western blotting to detect cell EGFR , ERK , AKT , IGF -1R expression and phosphorylation . Results SPC-A1 cells EGFR and K-ras gene mutation ; Dorsey with single-agent docetaxel or gefitinib Nepal than docetaxel with gefitinib application and first gefitinib erlotinib after sequential multi- West his race on cell growth inhibition no significant difference in the first Dorsey him after the game sequential gefitinib significantly enhanced growth inhibition them . Docetaxel and gefitinib , respectively, enhancement and inhibition of EGFR and ERK phosphorylation . EGFR and ERK phosphorylation induced by docetaxel significantly suppressed , but can not be applied at the same time gefitinib inhibit sequential application of gefitinib . Gefitinib inhibit EGFR and ERK phosphorylation can not be simultaneously or sequential application of docetaxel reversal . Docetaxel and gefitinib Niger different timing application had no significant effect on AKT phosphorylation . Docetaxel lowered expression of IGF-1R , gefitinib had no significant effect on IGF-1R expression . Compared to docetaxel , docetaxel sequential gefitinib had no significant effect on IGF-1R expression . Conclusion Dorsey race sequential gefitinib growth inhibition of erlotinib on EGFR wild -type lung adenocarcinoma cell SPC-A1 significantly enhanced mechanism may affect cell EGFR and ERK phosphorylation of AKT phosphorylation, and IGF-1R The expression has nothing to do .

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CLC: > Medicine, health > Oncology > Respiratory system tumors > Lung tumors
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