Objective To investigate the role and significance of neuropilin-2(NRP2)for regulating the angiogenesis of pancreatic neuroendocrine tumors(PNETs).Methods The NRP2 expression in pancreatic neuroendocrine tumer BON-1 cell line was intevened.The BON-1 cells cultural supernatants in the control group and interference group were used to treat human umbilical vein endothelial cells(HUVEC).CCK-8 was used to detect the cell proliferation,Transwell was used to detected the cell migration and the tubule formation test was used detect the pro-angiogenesis.Results The CCK-8 detection showed that there was no statistically significant difference in the supernatant treated HUVEC proliferations between the interference group and control group medium(P>0.05):the absorbancy in the control group was 0.35±0.04,while which in the interference group was 0.32±0.04.The Transwell test showed that the invasion ability of HUVEC treated with cultural supernatants in the interference group was weakened compared with the control group,the control group was(203±13)/hole,while the interference group was(100±10)/hole(P＜0.01);the tubule formation test showed that HUVEC tubular formation treated by cultural supernatant in the interference group was decreased,the control group was 40±5,while the interference group was 24±3(P＜0.01).Conclusion Interfering NRP2 expression of BON-1 cells can inhibit the vessel formation ability of co-cultured HUVEC,suggesting that NRP2 may have the pro-angiogenesis effect of PNETs,and may be a potential new target for the treatment of PNETs.

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.

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.

Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are exceedingly rare tumor,with an increasing incidence in recent years.According to the NANETS consensus guidelines for the diagnosis of neuroendocrine tumor,the algorithm for diagnosis of GEP-NENs includes clinical syndrome suggestive of NENs,biochemical testing,genetic testing,tumor localization by imaging and tissue diagnosis.GEP-NENs could be divided into functional versus non-functional based on the clinical manifestations.Radical surgery is the standard firstline therapy for limited-stage tumors.However,two-thirds of GEP-NENs patients are inoperable for tumor metastasis at initial diagnosis.For these advance staged patients,multidisciplinary treatment is the best choice,which includes surgery,chemotherapy,biotherapy,molecular targeted therapy,somatostatin receptor-targeted radionuclide therapy.Molecular targeted therapy may turn into a standard first-line therapy for its good curative effect in recent studies.

Objective To study the expression of splice variant of progesterone-induced blocking factor (PIBF) of healthy adult and hepatocellular carcinoma (HCC) patients. Methods Western blot was used to find out the expression in 3 normal livers and tumor and para-tumor tissue of 8 HCC patients. Use T Test to compare the difference. Immunohistochemistry was used to detect the expression in tumor and para-tumor tissue of 48 HCC patients. The splice variant of PIBF serum concentrations of 103 healthy adult, pre-operation and part of 5 days post-operation of 109 HCC patients was tested with ELISA. Result The expression of HCC tissue is lower than para-tumor tissue. The serum concentrations of healthy adult and HCC patients is 73.04 ± 6.29 ng/mL and 49.10 ± 4.07 ng/mL, and the difference was statistically significant (P=0.010). The analysis of blood concentrations of pre-operation and part of 5 days post-operation of 15 HCC patients indicate that the expression of pre-operation is lower than post-operation, and the difference was statistically significant (P = 0.008). Conclusion The splice variant of PIBF is low expressed in HCC tissue and serum. PIBF is a potential protein plays important role in cancer.

Objective: To examine the expression of glucocorticoid receptor in human colon cancinoma tis-sues and call lines and to explore the survival of colon cancer cell lines treated with dexamethasone alone or in combination with 5-Fu and L-OHP in a way of dexamethasone pretreatment or co-administration in vitro.Methods: The expression of glucocorticoid receptor was detected in 61 cases of colon cancer tissue samples and 4 types of colon cancer cell lines by immunohistochemistry. Apoptosis was detected by Hoechst33342 staining and flow cytometry. MTT assay was employed to detect the chemosensitivity of colon carcinoma cells to L-OHP and 5-Fu with dexamethasone pretreatment for 24 hours or co-administretion. Results: Positive GR expression was found in 57.3% colon cancer tissue samples and in Lovo and HCT-116 cell lines, not in HT-29 and SW-480. Apoptosis was detected in GR-expressed Lovo and HCT-116 cells at 72 hours after 1×10~(-4)mol/L Dex treatment, and the rates of apoptosis were higher than those in the control groups without Dex (P<0.01),GR-negative cells, HT-29 and SW-480 even treated with 1 × 10~(-4)mol/L Dex for 72 hours. Pretreatment and co-administration for Lovo cells with 1×10~(-4)mol/L Dex could decrease the IC50 of L-OHP from 13.7±1:1.3μg/mL to 5.9±0.6μg/mL and 4.8±0.7μg/mL, respectively. IC50 of 5-Fu was decreased from 72.2±8.1 μg/mL to 21.1±4.1μg/mL and 18.6±4.0μg/mL, respectively. Conclusion: There is expression of glucocorticoid receptor in part of colon carcinoma tissue samples and cell lines. Apoptosis does occur in GR-expressed Lovo and HCT-116 cells induced by dexamethasone in vitro. Pretreatment for 24h and co-administration with Dex can increase the chemosensitivity of Lovo cells to L-OHP and 5-Fu.

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.

Medical education on oncology is urgently enhanced in China.We analyse a host of questions in medical education on oncology in our country at present,and study didactical methods,goal and task on oncology education.

0.05).CONCLUSION:The domestic tropisetron hydrochloride is equivalent to the imported one in terms of the efficacy and safety in the treatment of cisplatin-induced nausea and vomiting.

BACKGROUNDNo chemotherapeutic regimen and agent are effective for most patients with advanced non-small cell lung cancer (NSCLC). This study is designed to evaluate the efficacy and toxicity of the combination of gemcitabine and cisplatin in the treatment of NSCLC..

METHODSSixty cases of NSCLC in stage III and IV were treated with gemcitabine 1200mg/m² by intravenous infusion on 1st and 8th days, and cisplatin 100mg/m² by intravenous infusion on 1st day or 30mg/m² by intravenous infusion on 1st and 8th days in a 28-day cycle. Each patient was treated at least for 2 cycles.

RESULTSAn objective response was obtained in 46.67% of patients (3 complete and 25 partial responses), whereas 22 patients had no change and 10 patients were progressive. The response rate was 57.14% in patients without prior chemotherapy and 22.22% in patients with prior treatment. Significant difference existed between the two groups (P < 0.05). The main toxicities were leukopenia and thrombocytopenia, but didn't influence the chemotherapy.

CONCLUSIONSThe combination of gemcitabine and cisplatin is a feasible, well-tolerated and effective scheme in the treatment of advanced NSCLC.