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Background and objective BIM gene is a member of the BCL-2 family, is involved in cell death. The aim of this study is to explore the relationship between BIM gene polymorphism and therapeutic efficacy in the retreatment advanced non-small cell lung cancer (NSCLC) with tyrosine kinase inhibitor (EGFR-TKI). Methods In the study, there were 123 patients who were diagnosed with advanced NSCLC in Zhejiang Province Cancer Hospital bewteen January 2009 to October 2012, all of who were received gefitinib and erlotinib therapy after failure to chemotherapy. We detected the genotype of peripheral blood leukocytes of patients with BIM gene polymorphism though polymerase chain reaction (PCR). Statistical analysis was performed by SPSS version 13.0. Results On the disease control rates, BIM gene with no polymorphism type was slightly better trend than polymorphism types in disease control rate DCR (75.5% vs 57.1%, χ2=2.931, P=0.087). Univariate analysis the median PFS, women were longer than men (6.9 months vs 4.5 months, χ2 =7.077, P=0.008). Non-smokers were longer than smokers (8.0 months vs 2.5 months, χ2 =15.277, P

Background and objective At present clinical researches has proven that the chemotherapeutic effect on advanced non-small cell lung cancer (NSCLC) has gotten to plateau. Biotherapy combined with chemotherapy could improve curative effect on advanced NSCLC obviously. The project is aiming at exploring the killing effect and the mechanism of rmhTNF-alpha in combination with gemcitabine on human lung adenocarcinoma cell line A549. Methods CCK-8 was used to detect the inhibition ratio of rmhTNF-alpha and gemcitabine cell line A549; cell curve of growth was used to illustrate the influence of rmhTNF-alpha and gemcitabine on the proliferation of A549; FCM was used to detect the cell cycle and the apoptosis ratio of cell line A549 treated with either rmhTNF-alpha or gemcitabine or those combined. The change in cellular morphology and cell ultra-micromorphology was observed by light microscope and transmission electron microscope respectively. Results The result of CCK-8 and cell curve of growth demonstrated that rmhTNF-? not only inhibited the proliferation of A549, but also enhanced the killing effect of gemcitabine; FCM showed that rmhTNF-? promoted S cell cycle arrest and reduced proportion of G2/M cell arrest; also showed different apoptosis ratio was most significant in the group of rmhTNF-? combination with gemcitabine; the changes of morphology was observed obviously by light microscope and transmission electron microscope. Conclusion rmhTNF-alpha enhances the the killing effect of gemcitabine on human lung adenocarcinoma cells A549 by inducing apoptosis and promoting cell cycle arrest.