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.

This article analyses the characteristics and current situation in oncology teaching,and studies the goals,task and methods on oncological probation.

Objective To investigate the relationship between the expression of vascular endothelial growth factor receptor 3 (VEGFR 3) and lymphangiogenesis in esophageal carcinoma. Methods VEGFR 3 expression in the esophageal carcinoma tissues from 73 cases was detected by RT PCR and immunobistochemical method. and the relationship between VEGFR 3 and lymphangiogenesis was analyzed. Results There was a statistically positive correlation between VEGFR 3 mRNA expression and lymph node metastasis in primary tumors ( P

Objective To investigate of the expression of vascular endothelial growth factor receptor 3 (VEGFR-3) and its relationship with the prognosis of esophageal carcinoma. Methods VEGFR-3 in 156 cases of esophageal carcinoma tissues was detected by immunohistochemistry. The follow-up data for 3 years in 47 cases were analyzed. Results The VEGFR-3 expression in esophageal carcinoma tissues with lymph node metastasis was higher than that in those without lymph node metastasis. VEGFR-3 expression was associated with the clinicopathological stages. Analysis of the follow-up data also showed that there was a statistically positive correlation between VEGFR-3 expression and lymph node metastasis in primary tumors (P

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.

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.

Objective Taking CNE-2Z multicellular spheroids (MCSs) as the simulation of solid tumors, to investigate the role of SAPK/JNK signaling pathway in multicellular resistance to radiotherapy for human nasopharyngeal carcinoma (NPC). Methods Human NPC cell line CNE-2Z were cultured into multicellular spheroids by using liquid overlay technique, then divided into control MCSs, irradiated MCSs (average dose in one minute: 2 Gy), sp-600125(a specific inhibitor for SAPK/JNK signaling pathway)+irradiated MCSs, sp-600125+MCSs. Western blotting was employed to analyze the activity of SAPK/JNK signaling pathway in MCSs, and the expression of Caspase-3 protein before and after sp-600125 treatment; X-ray induced cell apoptotisis in MCSs before and after sp-600125 treatment was detected by TUNEL. Results The level of SAPK/JNK phosphorylation in MCSs was a dynamic course after radiation, and the phosphorylation peaked at 2 h after irradiation; The apoptotic rate of MCSs (P

Objective To investigate the effects of transfection of chemokine receptor CXCR4 antisense-RNA on the functional expression of VEGF-C mRNA and the invasive ability of colon cell line HT-29 in vitro.Methods PCR primers were designed according to the coding sequence of CXCR4 gene.EcoR Ⅰ and BamH Ⅰ recognition sequences and cutting sites were added to the 5' end of the antisense primer.The purified PCR fragment was retro-inserted into the cloning site of eukaryotic expression vector pcDNA3.1(+).The pcDNA3.1(+)for CXCR4 antisense-RNA was transfected into colon cancer HT-29 cells by liposome transfection.The expression of VEGF-C mRNA was detected by RT-PCR.The expression of CXCR4 protein was determined by Western blot.At the same time,cell growth kinetics was assessed by MTT assay,and in vitro invasive ability was assessed with Boyden chamber.Results CXCR4 antisense-RNA recombinant was successfully constructed.The expression of VEGF-C mRNA in antisense-CXCR4 transfected(HT-29tran)group decreased by 54.2%,while the expression of VEGF-C mRNA in vacant-transfected(HT-29KZ)group only decreased by 9.4% campared with non-transfected(HT-29)group.The difference between the two groups mentioned above was remarkable(P

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 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