0.05) was observed in the expression of PDI in fluoride treated groups, and the expression of XBP-1 in 10-80 mg/L groups was significantly higher with a dose-dependent manner, and in 2.5-80 mg/L groups, the expression of BIP/?-actin was up-regulated (P

Arsenic compounds are poisonous to organisms,which may induce chromosome aberration and gene mutation of cells.Arsenic compounds may also change the gene functions and cause carcinoma.After exposure to arsenic compounds,gene expressions in some cells were changed.The results of some molecular biology studies showed that both prokaryote and eukary-ote had responses to arsenic compounds at molecular levels.It will be important for unveiling the molecular mechanisms of ar-senic compoundseffects on cells and organisms and the arsenic-resistance of various cells and organism by studying the inter-actions between arsenic compounds and genes.In addition,it was recently found that arsenic trioxide could induce cell apoptosis by various cellular signal transduction pathways.

0.05),while the activities of SOD of bone tissue were lower(P

Objective To study the effects of arsenic compounds on metallothionein-3 gene expression in human normal hepatic cells. Methods cDNAs were cloned by SMART method. Bioinformatics was utilized to analyze the homologue, chromosomal localization, structure and encoding protein of the cloned gene and the trans-membrane information of the encoding protein. Metallothionein-3 gene expression level in L-02 cell line treated by arsenite was determined by cDNA microarrays. Results Metallothionein-3 cDNA gene was cloned and located in the chromosome 16q13. The results of bioinformatics analysis showed that the protein encoded by metallothionein-3 gene could cross the biologic membrane. Metallothionein-3 gene expression up-regulation in human normal hepatic L-02 cell line was found by cDNA microarrays in the early stage after the cells being exposed to arsenite. Conclusion The results of this study showed that the human metallothionein-3 gene was arsenic related gene and this gene might play a vital role in the detoxification metabolism of arsenic compounds at early stage.

AIM:Based on comparative genomic hybridization(CGH) data,to construct tree model of esophageal carcinoma and to explore mechanism of multigene involved,multistep development and multipathway progression during esophageal carcinogenesis.METHODS:Using the software developed by Desper et al,tree models of esophageal carcinoma were constructed according to the CGH data of 78 esophageal carcinoma patients.RESULTS:Tree models for esophageal carcinoma suggested that there were-4p,-9p,-18q,+7p,+8q,+17p,+17q,+20p,+20q nine nonrandom genetic events,and +7p、+8q and +20q might be important early events in esophageal carcinogenesis,indicating that there might be cancer-related genes in these chromosomal arms.CONCLUSION:Tree models based on CGH data of esophageal carcinoma imply the process of multigene involved,multistep and multipathway progression.The tree models also give the direction to search for esophageal cancer-related genes.

Objective To assess the outcomes of involved field irradiation (IFI) and elective nodal irradiation (ENI) in patients older than 70 years with esophageal squamous-cell carcinoma(SCC) receiving radical IMRT,and to determine whether IFI is feasible in these patients.Methods Totally 79 patients older than 70 years diagnosed with SCC of esophagus without distant metastases were collected.48 patients were received IFI,and the other 31 patients were treated with ENI.With a median follow-up time of 24 months,disease-free survival,overall survival,patterns of failure,irradiated lung dose and radiation pneumonitis were observed and compared between IFI and ENI groups.Results In IFI and ENI arm,the disease-free survival rates of 1,2,3 years were 60.4％,34.9％,29.7％ and 64.5％,54.0％,35.0％,respectively(P ＞0.05).The 1-,2-,and 3-year survival rates were 72.9％,43.4％,31.5％ for the IFI arm,and 73.0％,53.0％,38.3％ for the ENI arm(P ＞ 0.05).The ENI arm had a tendency to expand survival,but the two arms had no significant difference (P ＞ 0.05).The patterns of failure also had no difference between the two arms.Distant failure,local failure,uninvolved nodal failure in IFI arm were 22.9％,27.0％,4.2％,while in ENI arm were 25.8％,0,19.4％,all of them had no significant difference (P ＞ 0.05).However,the lung V5,V20,mean lung dose in ENI arm were higher than that in IFI and all of them had a significantly difference (t =4.66,29.90,15.63,P ＜ 0.05).The radiation pneumonitis rates were higher in ENI than in IFI arm.The rates of degree 1-2 and degree 3 were 22％,19％,and 13％ and 4％ in the two arms,respectively,with a significantly difference(x2 =4.55,4.77,P ＜ 0.05).Conclusions It is feasible that IFI for definitive IMRT in the elderly patients older than 70 years with SCC,because it got similar disease-free survival and overall survival but with less lung doses along with decreased radio-pulmonary lesion when compared with ENI.

Objective To construct a recombinant lentiviral expression vector for RNA interference (RNAi) of human Snail gene and to study its effects on the proliferation and invasion of nasopharyngeal carcinoma cell line 5-8F. Methods The effective sequence of short hairpin RNAs (shRNA) targeting Snail gene was designed and cloned into the linear pLVTHM vector after enzyme digestion. After confirmation by DNA sequencing, 5-8F cells were infected with the viral supernatants. The cells with stable Snail gene knock-down were separated by fluorescence activated cell sorter (FASC). The expression of Snail mRNA was detected by real time RT-PCR. MTT and cell invasion assay were used to detect the proliferation and invasion of 5-8F cells after plVTHM-siSnail transfection. Results The lentivirus vector plVTHM-siSnail was constructed successfully. The separated 5-8F-plVTHM-siSnail exhibited significant knock-down of Snail mRNA expression. Slower proliferation and decreased cells to permeate through the Matrigel were found after plVTHM-siSnail transfection (P

Site-directed mutagenesis method was used to introduce two desired mutations, which were confirmed by DNA sequencing, into mouse complement receptor Type II gene(MCR2). Then the constructed eukaryotic expression vectors containing wild type mouse CR2/1(wtMCR2/1), mutant type mouse CR2/1 (mtMCR2/1) and human CR2 (hCR2) cDNA were transferred into mouse SP2/0 cells by electroporation. After two-week screening by G418, the stably transfected clones were obtained. Several ways including PCR, RT-PCR, and immunohistochemistry were utilized to screen those clones with interesting genes integrated and expressed. Then Epstein-Barr virus(EBV) was used to infect these transfected cells and EBER-1 (EBV encoded RNAs) hybridization results showed that only hCR2 and mtMCR2 transfected SP2/0 cells could be infected by EBV, but positive rate of the former was much higher than the latter. This study sets groundwork for elucidating the mechanism by which EBV enters the cells and for establishing the animal model of EBV-related nasopharyngeal carcinoma (NPC).

Objective To screen potential genes associated with drug resistance and multidrug resistance. Methods Microarray with 8000 genes was used to detect the different expression of 5-8F cells and 6-10B cells. Subsquently, genes of drug resistance and multidrug resistance were screened by MILANO online programme. Semiquantitative RT-PCR was utilized to confirmed the reliability of differentially expressed genes. Results 283 genes were identified the differential expression. Of these, 85 genes were shown to be upregulated and 98 downregulated. After the analysis of MILANO, 4 genes including UGT1A9 (15.85 folds),MVP(6.77 folds), CAV1(2.49 folds) and HIF1A(2.67 folds) with higher expression in 5-8F cells were found to be likely associated with drug resistance and multidrug resistance. Subsquently, semiquantitative RT-PCR confirmed the reliability of differential expression of these 4 genes. Conclusion Differentially expressed genes shown in NPC 5-8F cells compared to 6-10B cells with the identification of online MILANO program analysis are likely associated with drug resistance and mnltidrug resistance of NPC cells with the ability of metastasis.

Objective To observe the effect of three dimensional conformal radiotherapy combined capecitabine in treatment of rectal cancer. Methods Sixty patients with advanced rectal carcinoma from January 2010 to January 2011 were selected, 32 cases with three dimensional conformal radiotherapy combined capecitabine establishment as the ob-servation group, 28 cases with simple radiotherapy establishment as the control group, the total effective rate, disease control rate, the rate of local recurrence, distant metastasis rate, adverse reaction rate were compared between two groups. Results After 4 cycles of therapy, the clinical total effective rate of observation group was 53.1%, the control group was 28.6%, there were significant differences (P<0.05). The disease control rate of observation group was 90.6%, the control group was 67.9%, there were significant differences(P<0.05). Compared with control group, the local recur-rence rate and the rate of distant metastasis of observation group had statistically significant difference (P<0.05). Con-clusion Concurrent three dimensional conformal radiotherapy combined with capecitabine in the treatment of rectal cancer has curative effect, good safety, can reduce the recurrence rate and distant metastasis rate and increase the sur-vival rate of patients.