Objective To understand the roles of JAK STAT pathway in the process of differentiation of human cord blood CD34 + hematopoietic stem cells into dendritic cells (DCs) by detecting the expressions and activation of JAK2 and STAT5. Methods CD34 + hematopoietic stem cells isolated from human umbilical cord blood and cultured for two weeks were induced to differentiate into DCs in vitro . Total cellular JAK2 and STAT5 and tyrosine phosphorylated protein stimulated by granulocyte/macrophage colony stimulating factor (GM CSF) at different time points (0, 7, and 14) during DC differentiation were detected by Western blotting. Results The amount of JAK2 protein was similar at 0, 7, and 14 d without GM CSF stimulation. With the differentiation of cells into DCs, the amount of tyrosine phospho JAK2 induced by GM CSF increased markedly. Both total cellular and tyrosine phospho STAT5 expression increased markedly during DC differentiation. Maximal tyrosine phospho STAT5 expression was later than JAK2. Conclusion JAK STAT pathway may take part in the signal mechanism of DCs differentiation from CD34 + hematopoietic stem cells stimulated by GM CSF.

Objective To explore the clinical efficacy of intranasal endoscopic turbinate fracture relocation press in treatment of chronic hypertrophic rhinitis.Methods According to digital table,66 patients with chronic hypertrophic rhinitis were randomly divided into two groups.33 cases in the observation group were treated with endoscopic sinus lateral fracture crush,33 patients in the control group received inferior turbinate submucosal injection of sclerosing treatment.The clinical effect was compared between the two groups.Results The total effective rate of the observation group was 93.9％,which was significantly higher than 72.7％ of the control group (x2 =6.23,P ＜0.05).The average nasal recovery time was (35 ± 12)d in the observation group,which was significantly shorter than (64 ± 21) d in the control group (t =1.74,P ＜ 0.05).The SCT test results had statistically significant differences between the two groups before treatment and 3 months after treatment (t =3.21,2.85,all P ＜0.05).After treatment,the difference was statistically significant between the two groups (t =2.13,P ＜ 0.05).Conclusion Endoscopic turbinate fracture relocation squeezing surgery in the treatment of chronic hypertrophic rhinitis was satisfied.

Objective To explore the distributive changes of PIDD protein in HT29 cells stimulated by 5-fluorouracil(5-FU),and the influence of the PIDD protein interfered by small interference RNA(siRNA) on the drug resistance of HT29 cells in vitro.Methods siRNA was used to interfere the PIDD expression,and HT-29 cells were treated with 5-FU.Western blotting was employed to detect the PIDD expression before and after interference.The distribution of PIDD in nucleus and cytoplasm after 5-FU treatment was also detected.Changes in drug sensitivity of HT-29 cells to 5-FU were determined with MTT assay and IC50 values were evaluated.Results PIDD protein was expressed mainly in the cytoplasm before 5-FU stimulation,and it migraded into the nucleus after stimulation.Western blotting showed that the total PIDD expression and the expression both in cytoplasm and nuclei decreased significantly after RNA interference,and no increase of the total PIDD and that migrated into nucleus was found even after 5-FU stimulation.It was found that in the transfection group(cells were incubated 12h after being transfected with PIDD-360),normal group(cells without treatment) and control group(cells were incubated 12h after being transfected with negative transfection reagent),the IC50 values of cells treated with 5-FU were 0.23?0.06?g/ml,2.71?0.70?g/ml and 2.78?1.03?g/ml,respectively.The IC50 value declined significantly in transfection group compared with that of both the normal group and control group(P

0.05).IGFR-1? expressed in all the 6 cell lines,with the highest expression in SW480(P0.05),but a gefitinib-induced and dose-dependent increase in p-IGFR-1?,not IGFR-1?,expression was observed in HT29 cells(P0.05),but the expression of IGFR-1? was higher in HCT116 than in Lovo and HT29(P

Objective To evaluate the inhibitory effects of gefitinib on the growth of colon carcinoma cells with different degree of sensitivity,and the activated status of epidermal growth factor receptor(EGFR) associated signal pathway proteins.Methods The colon carcinoma cell lines(Lovo,HCT116 and HT29) were treated with 10?mol/L of gefitinib,and flow cytometry was employed to detect the cell cycle and apoptosis.Another portion of cells were treated with 50ng/ml of epidermal growth factor(EGF) or 5?mol/L or 10 ?mol/L of EGF+gefitinib,and Western blotting was used to determine the expressions of PTEN,EGFR,AKT and MAPK,as well as their corresponding phosphorylated proteins,p-EGFR,p-AKT and p-MAPK.Results After being treated with gefitinib,the G1 phase cells and apoptosis rate increased remarkably in Lovo,slightly in HT29,while no significant change was found in HCT116.With the treatment of EGF alone,the expressions of p-EGFR,p-AKT and p-MAPK increased significantly in Lovo and HT29 cells(P0.05).Conclusions The growth of colon carcinoma cells,which are resistant to gefitinib,is not dependent on EGFR,and the activated status of signal pathway of the gefitinib-resistant cells will not be inhibited as the EGFR is blocked.The present findings suggest that sensitivity of colon carcinoma cells to gefitinib relies on EGFR as well as the activation of its downstream signal pathway.

Objective To investigate the relationship between the sensitivity of colon carcinoma cells to epidermal growth factor receptor(EGFR) inhibitor,gefitinib,and the downstream proteins of EGFR.Methods The expressions of EGFR proteins of 6 colon carcinoma cell lines(Lovo,HCT116,HT29,LS174T,SW480 and SW620) were determined with immunocytochemistry staining.The inhibitory effects of gefitinib on the growth of colon carcinoma cells were assessed by MTT,and the expression levels of Akt and MAPK as well as their phosphorylated forms(p-Akt and p-MAPK) were assessed by Western blotting.Results EGFR protein expressed in all the Lovo,HCT116,HT29,LS174T and SW480 cells,and the highest expression was found in Lovo cells,but not in SW620 cells.Lovo cells showed the highest,HT29 and SW480 cells showed moderate,sensitivity to gefitinib,while the others showed more or less resistance to gefitinib.No significant difference was found between the growth inhibition and IC50 values among the 6 cell lines despite of being treated with fetal bovine serum or EGF.Akt protein existed in all the cell lines without notable difference.Lovo and SW620 cells showed the least of p-Akt expression(P

Objective To explore the effects and the underlying mechanisms of inhibiting three kinds of DNA methyltransferases(DNMT1,DNMT3a and DNMT3b) on the re-expression of cancer/testis antigen(CTA) in hepatic cells.Methods Transient transfection of HepG2 cells with siRNA was targeted against DNMT1,DNMT3a and DNMT3b(DNMT1+3a+3b),DNMT1 and DNMT3a(DNMT1+3a),DNMT1 and DNMT3b(DNMT1+3b),DNMT3a and DNMT3b(DNMT3a+3b),respectively.The other batch of cells was treated with 5'-aza-deoxycytidine(5-aza-dC) as positive control.Real-time PCR and Western blotting were used to detect the expressions of DNMTs and CTAsm,and the promoter methylation of partial CTA genes was detected with methylation specific PCR(MSP).Results Expressions of DNMT1,DNMT3a and DNMT3b declined significantly after siRNA interference in HepG2 cells.Two CTAs,CT10 and SSX1,re-expressed in the cells transfected by DNMT1+3a and DNMT1+3b.MAGE1 and MAGE3 were equally expressed in all cells despite been transfected or not.Demethylation occurred in the promoter region of CT10,while the promoter region of MAGE1 was in a state of unmethylation.Conclusions In HepG2 cells,CTA promoter can be demethylated via interference of DNMTs,which may lead to the re-expression of CTA that was originally unexpressed due to methylation.

Objective To observe the inhibitory effect of Gefitinib,a selective oral epidermal growth factor receptor tyrosine kinase inhibitor,on the growth of human colon cancer cells,and investigate the relationship between the sensitivity of colon cancer cells to Gefitinib and PIEN expressions.Methods The inhibitory effects of Gefitinib on 6 kinds of colon cancer cells(Lovo,HCT116,HT29,Lsl74T,SW480 and SW620),the levels of PTEN mRNA in different colon cancer cells.and PTEN protein expressions in colon cancer cells were detected by MTT assay,RT-PCR and Westem blot,respectively.Results The inhibitory effects of Gefitinib on the 6 colon cancer cells in vitro varied a lot.When the concentration of Gefitinib was 1 μmol/L,LoVO cells had the most sensitivity to Gefitinib with an IC50＜10μmol/L;HT29 and SW480 had moderate sensitivity,and the IC50 ranged from 10 μnol/L to 100 μmol/L;HCT116,LS174T and SW620 were insensitive to Gefitinib,and their IC50＞100 μmol/L.All the colon cancer cell lines exhibited PTEN mRNA and protein expressions.Conclusions PTEN mRNA andprotein expressions might not be associated with the inhibitory effects of Gefitinib on the growth of colon cancer cells.The expression of PTEN can not be taken as the indication of the sensitivity of colon cancer cells to Gefitinib.

Objective To evaluatethe effect of mTORC1 inhibitor on the proliferation in human pancreatic neuroendocrine tumors(pNET)cell line BON,to explore the function of glutamine metabolism in it.Methods In vitro cultured human pancreatic neuroendocrine tumors(pNET)cell line BON,BON cells were treated with different concentrations of rapamycin(1,5,10,25,50, 100 nM)for 12,24 h.Then CCK-8 assay are used to calculate the growth inhibitory rate.Rapamycin treated with BON 12 h,test the glutamine uptake level compared with control.Then deprive of glucose and/or glutamine,CCK-8 assay were used in observation of cell proliferation,cell cycle distribution was analyzed by flow cytomety.Results Rapamycin significantly inhibited the growth of BON cells in a time-and dose-dependent manner(P <0.05).Meanwhile,rapamycin can reduce the glutamine uptake level compared with control.BON obviously depends on glutamine for growth,without glucose and glutamine group have obvious difference in growth rate(P <0.05).Conclusion mTORC1 inhibitor can inhibit BON cells proliferation and influence the glutamine uptake lev-el.suggesting that mTORC1 inhibitor might inhibit BON cells proliferation by influenced the glutamine metabolic pathway.

Standardized rotary residency training is an important part of clinical medical education. Traditional clinical teaching can't meet the rapid development of oncology medicine. In the rotary residency training in oncology department, we put forward the problems encountered in clinical practice, stimulate the interest and initiative of residence, the PBL teaching model is combined with the evidence-based medicine in the teaching process through the relevant training, literature review and discussion. By standardizing the treatment concept the residence's understanding of the basic theory and frontier knowledge of oncology was improved, the thinking innovation and clinical practice ability of the residency doctors were enhanced.