Lung cancer remains the leading cause of cancer death in the worldwide.Approximately 45% of patients present with stage III disease.For patients with unresectable stage IIIA/B disease,Several clinical trials demonstrated concurrent chemoradiotherapy was superior to TRT alone and sequential chemoradiotherapy.Chemoradiotherapy is a standard treatment for unresectable locally advanced non-small cell lung cancer(NSCLC),Cisplatin-based chemotherapy with concurrent thoracic radiotherapy yields a 5-year survival rate of approximately 15% for patients with unresectable locally advanced NSCLC.Despite a substantial number of clinical trials,The most effective chemotherapy combination,the use of induction or consolidation chemotherapy in addition to the concurrent portion of therapy,and the optimal dose of chemotherapy with concurrent TRT have yet to be determined.In addition to evaluating optimal sequencing strategies of combined modality therapy,current investigations are also focusing on the integration of novel agents,including chemotherapeutic and targeted therapies.Currently ongoing trials involving novel approaches are reviewed here.

Objective: To construct and identify a lentiviral vector harboring RNAi sequence targeting the human high mobility group A1(HMGA1) gene.Methods: The effective sequence of siRNA targeting the HMGA1 gene confirmed in our previous study,the complementary DNA containing both sense and antisense Oligo DNA of the targeting sequence was designed,synthesized and cloned into the pGCL-GFP vector diced by the restriction enzyme of HpaⅠ and XhoⅠ,which contained the U6 promoter and green fluorescent protein(GFP).The resulting lentiviral vector containing HMGA1 shRNA was named LV-sh HMGA1 and confirmed by PCR and DNA sequencing.A total of 293T cells were cotransfected with LV-sh HMGA1,pHelper 1.0 and pHelper 2.0.All the virus stocks were produced by Lipofectamine2000-mediated transfection.The titer of the virus was tested according to the expression level of GFP.Results: PCR analysis and DNA sequencing demonstrated that the RNAi sequence targeting the human HMGA1 gene was successfully inserted into the lentiviral vector.The titer of the recombinant lentiviral vector was 5?107 TU/ml.Conclusion: The successful construction of the lentiviral vector of HMGA1 has prepared the ground for further studies on the functions of the HMGA1 gene with the RNAi technique.

Objective To determine the content of aconitine-type alkaloids in Bitongxiao Ointment,and to control the limits of aconitine-type alkaloids in the ointment.Methods Acid-dye colorimetry was employed and methodology was examined for linear range,average recovery,precision,exclusivity and stability.Results The method has a good precision and stability.The linear range of aconitine-type alkaloids was in 0.111 9～0.714 mg(r=0.999 3),and the average recovery was 97.4 %.Conclusion The method is accurate,reliable,simple,can be used to determine the content of aconitine-type alkaloids in Bitongxiao Ointment.

AIM:To investigate the activation and inactivation of nuclear factor kappa B(NF-κB)when tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)is applied to induce the apoptosis of androgen-independent prostate cancer cell line PC-3M.METHODS:After the treatment of TRAIL or LPS at different doses,we tested the nuclear translocation of NF-κB by cell immunohistochemical staining and electrophoretie mobility shift assay(EMSA),and evaluated the level of IκB by RT-PCR under pyrrolidine dithiocarbamate(PDTC)treatment.RESULTS:EMSA and cell immunohistochemical analysis showed that the translocation of NF-κB was significantly activated when PC-3M cells were treated with TRAIL or LPS(P＜0.05).The pretreatment of PDTC upregulated the expression of IκB and blocked the nuclear translocation of NF-κB.CONCLUSION:TRAIL remarkably stimulates the activation of nuclear NF-κB in androgen-independent prostate cancer cells.On the other hand,the translocation of NF-κB can be significantly and efficiently inhibited in PC-3M cells by pretreatment with PDTC.The increased expression of IκB might be a clue for this inhibition,which means the possible way to enhance the effect of TRAIL in the apoptosis of prostate cancer cells.