Chemotherapy for lung cancer is expected to prolong the survival of lung cancer patients. multidrug resistance is considered to be a major cause of failure of treatment. Many multidrug resistance mechanisms have contributed to lung cancer drug resistance, such as P glycoprotein (P gp), multidrug resistance associated protein (MRP), lung resistance related protein (LRP). The drug efflux pump mechanisms are the focus of recent researches.

Objective To explore the effects of antisense vector of annexinⅡ gene on the growth of SPC A 1, a human lung cancer cell line. Methods The total RNA was isolated from human lung cancer cell line SPC A 1 and the target DNA fragments were amplified by RT PCR. The antisense expression vector was constructed by double restriction endonuclease cleavage directional clone method. Annexin Ⅱ antisense expression vector was introduced into SPC A 1 cells by liposome transfection reagent. The expression of annexin Ⅱ mRNA was analyzed by semi quantitative RT PCR. The effects of antisense vector of annexinⅡ gene on the growth of SPC A 1 were observed. Results The antisense vector of annexinⅡ gene was constructed and introduced into SPC A 1 cells successfully. Semi quantitative RT PCR showed that the annexin Ⅱ mRNA expression reduced by about two thirds in the transfected cells as compared with that in the untransfected cells. Compared with the untransfected cells, transfected cells decreased significantly in cell growth, clone formation efficiency in plating and DNA synthesis. Cell cycle was blocked in G 0 G 1 phase. Conclusion Annexin Ⅱ could promote the growth of lung cancer cells and may be helpful for the development of lung cancer.

0.05)。The median time to progression (mTTP)was 5.8 months in XELOX group and 5.7 months in FOLFOX4 group. The median survival time (MST) was 10.0 months in XELOX group and 9.8 months in FOLFOX4 group, The toxicities were well tolerated,The incidence of grade Ⅲ+Ⅳ nausea and vomiting was significantly lower in XELOX group than in FOLFOX4 group (P0.05).Conclusions:Both of the two regimens were feasible, well tolerated and effective in treatment of advanced gastric cancer。XELOX regimen may be safer than FOLFOX4 regimen,especially in elderly patients or patients with ECOG PS of 1 to 2.

Background and purpose:It has been shown that chemotherapy could improve the quality of life and prolongation of survival time of the patients with advanced gastric cancer. There is still no standard chemotherapy regimen for advanced and metastatic gastric cancer, and regimens with high efficacy and safety are scare. Toxicities are considered to be limiting factors and in? uence the quality of life in the patients with advanced gastric cancer. The purpose of this study was to investigate the effi cacy and toxicity of docetaxel(DOC) in combination with oxaliplatin(OXA) as fi rst-line treatment in advanced gastric cancer and try to fi nd a regimen that would be more tolerable without deterioration of treatment response. Methods:48 patients with advanced gastric cancer were treated with docetaxel 35 mg/m2, ivgtt, d1,d8 combined with oxaliplatin 130 mg/ m2,ivgtt,d1 ;repeated every 3 weeks (one cycle) ,The effect was evaluated after two cycles. The effi cacy and toxicity were evaluated according to WHO standard. Results:48 patients could be evaluated for clinical response. Complete response in 3 pts and partial response in 24 pts were observed with an overall response rate of 56.25%, median time to progression (MTTP) was 5.6 months and median overall survival (MST) was 11.8 months. The most common toxicities were bone marrow suppression, peripheral neuritis, nausea and vomiting. All of them are reversible. Conclusion:Combining weekly docetaxel and oxaliplatin is an effective and well tolerated alternative treatment in advanced gastric cancer and has yielded promising results.

Objective To establish lung adenocarcinoma drug resistance cell strain induced by cis-diaminodichloroplatin and investigate the biologic characteristics and chromosome karyotype of cell strain.Methods Large dosage impact and step by step inducing method were used to establish A549 and SPC-A-1 drug resistance cells: A549/CDDP and SPC-A-1/CDDP.MTT was used to detect the cell drug resistance index. Bioluminescence was used to detect the energy metabolism.Cell cycle was analysed by flow cytometer.The differential staining technique and SKY were used to analyze the chromatosome of A549/CDDP and SPC-A-1/CDDP.Results The drug resistance index of A549/CDDP and SPC-A-1/CDDP were 14.0 and 12.0. The content of ATP,ADP and AMP decreased significantly.The cell cycle of A549/CDDP and SPC-A-1/CDDP were of no notable changes.The results of the differential staining technique and SKY showed that the chromatosome of A549/CDDP and SPC-A-1/CDDP had several derivative chromosomes.Both cells had the same derivative chromosome: der(21)t(21;22).Conclusion CDDP can induce lung adenocarcinoma cell strain drug resistance.The derivative chromosome,including der(21)t(21;22) may have relationship with the drug resistance of cell strains.

Objective To analyze the unbalanced state of hereditary material of squamous carcinoma, adenocarcinoma and other lung cancers. Methods Fifty-five patients suffered from lung cancer were included in this study, including 24 of squamous carcinoma, 13 of adenocarcinoma, 5 of adenosquanous carcinoma, 8 of bronchioalveolar carcinoma, 4 of small cell lung cancer and 1 of atypical carcinoma. The technology of comparative genomic hybridization (CGH) was used. The normal DNA was obtained from 20 healthy male volunteers. Results The common extension region of squamous carcinoma was 2q, 5p, 11q and 22q, and the common deletion region was 1p, 4q, 5q, 6q, 8p, 9p, 10q, 11p, 13q, 18q and 21q. The common extension region of adenocarcinoma was 5p, 8q and 11q, and the common deletion region was 10p and 19. Conclusion The hereditary material of squamous carcinoma, adenocarcinoma and other lung cancers was unbalanced. The extension and deletion of chromatosome were the base of the occurrence of different lung cancer.

Objective To investigate whether sialic acid disaccharides, specificity agglutinins and neuramidinases could inhibit Pseudomonas aeruginose infection in rat trachea vulnerated by hydrochloric acid. Methods One hundred and forty male Wistar rats were vulnerated by hydrochloric acid through intratracheal instillation and then inoculated by Pseudomonas aeruginose admixed Sial ?2,3-Gal, Sial ?2,6-GalNAc, Maackia amurensis agglutinin, Sambucus nigra agglutinin, specificity ?2,3-neuramidinase or non-specificity neuramidinase respectively. Thirty minutes and 48 h after inoculation, whole trachea of 8 rats in each group was weighed, homogenated, and quantitative bacterial culture was performed while whole trachea of another 2 was fixed in 10% methanol, embedded with paraffin and HE stained. Results Sial ?2,3-related disaccharide, agglutinin and neuramidinases could decrease colony count of trachea 30 min after inoculation remarkably. But only Sial ?2,3-Gal and neuramidinases could obviously decrease colony count 48 h later. Sial ?2,6-related substrances have not analogical effects. Conclusion Sial ?2,3-related substrances could interfere Pseudomonas aeruginose binding/multiplication in the trachea, especially Sial ?2,3-Gal and neuramidinase.

Intensity-modulated radiation therapy (IMRT)is a more advanced radiotherapy technique than routine radiotherapy,and has been effectively utilized in the treatment of nasopharyngeal carcinoma (NPC).Rradiotherapy alone has disappointing effect to local advanced cases.Nevertheless,chemoradiotherapy provides long term survival.Chemoradiotherapy is becoming the standard therapeutic regimen for local advanced NPC.But different ways of chemomdiotherapy such as induction,concurrent,adjuvant chemotherapy still need to be defined.

Purpose:To study the biological effects of high secreted canstatin on human umbilical vein endothelial cells (HUVEC) and tumor model. Methods:Hypoxic responsive elements (HREs) were inserted in the upper stream of canstatin cDNA of a recombinant vector we constructed in a former research. The new recombinant vector named pCMV-3HRE-CEAS-Cans was transferred into A549 cells by cationic liposome; canstatin mRNA expression in the transformed cells under oxic and anoxic condition was detected by Taqman PCR. Then we designed a co-cultured assay: HUVECs were co-cultured with recombinant vector transformed A549 cells with Transwell plates, and the proliferation and apoptosis of co-cultured HUVECs were evaluated with 3H-thymidine incorporation method, TUNEL method respectively. Finally the vector was introduced into tumor tissues of lung cancer-bearing nude mice, and the biological activity in the tumor tissues was tested by micro-vessel count (MVC). A vector of canstatin we constructed before was used as controls in above experiments.Results:The pCMV-3HRE-CEAS-Cans vector was successfully constructed and transferred into A549 cells. canstatin mRNA was detected both in the recombinant vector transformed A549 cells and the pCMV-CEAS-Cans transformed A549 cells, moreover the expression of canstatin in the new vector transformed A549 was significantly higher than that of the controls under hypoxic condition. ~(3)H-TdR intake rate of HUVECs was decreased markedly, and a large amount of them underwent apoptosis when they were co-cultured with recombinant vector transformed A549 cells. Significant differences of ~(3)H-TdR intake rate and apoptotic rate of co-cultured HUVEC were found between pCMV-3HRE-CEAS-Cans group and any of the controls (P

To study the possibility of enhancing IFN ? level in the lung of rats by gene transfection. The recombined IFN ? expression vector in eukaryotic cell was constructed, and it was transfected into lungs of immunocompromised rats. The expression of pLXSN IFN and pLXSN in the genomic DNA of the transfected cells was investigated, and the level and activity of IFN ? in the BALF and sera was assessed. The results showed that the sequence of the IFN ? gene in the constructed recombinant pLXSN IFN eukaryotic cell was the same as that of the IFN ? of rats found in the Gene Bank. The band of transfected plasmid was found when the eletrophoresis analysis of PCR product of genomic DNA of the transfected cells in BALF was done. It could still be the found 21 days after transfection. The level and activity of IFN ? in the BALF of the transfected pLXSN IFN group were markedly higher than those of transfected pLXSN group.On the other hand, the level and activity of IFN ? in sera showed no difference between the two groups. It was suggested that the constructed recombinant IFN ? exprossion vector in eukaryotic cell could be transfected into the cells of the lungs of rats successfully, inserted into the genomic DNA, resulting in active secretion of IFN ?, and prolongation of its expression.