ABSTRACT
Objective To study the effect and toxicity of COX-2 selective inhibitor, celecoxib, plus doxetaxel + epirubicin regimen for LABC as neoadjuvant chemotherapy. Methods 59 women with LABC staged ⅡB～ⅢB were allotted and randomly divided into 2 groups: the control group consisted of 29 patients and with the dosage: doxetaxel (75 mg/m2, d1), epirubicin(75 mg/m2, d1) every 3 weeks; the experiment group consisted of 30 patients and with the dosage: doxetaxel (75 mg/m2, d1), epirubicin(75 mg/m2, d1) and celeeoxib (40Omg, twice daily, d1～21) every 3 weeks. After 2 cycles, the efficacy and toxicity of each group were evaluated. Results The control group achieved an overall response rate (RR) of 72.41%(21/29), and consisted of clinical complete remission (cCR) 2 cases, partial remission (PR) 19 cases, stable disease (SD) 8 cases; the experiment group achieved a RR of 80.00 %(24/30), and consisted of eCR 3 cases, PR 21 cases, SD 6 cases. Both of the group had no pathological complete remission (pCR) and progressive disease (PD) case, and the difference of RR between 2 groups showed no statistical signifieance(χ2=0.469, P=0.493). There was no difference of the diameter of tumor between 2 groups before neoadjuvant ehemotherapy(t=0.569, P= 0.570), but showed statistieal significance after neoadjuvant chemotherapy (t=7.300, P=0.000). Incidence of myalgia and arthralgia of the experiment group was lower than that of control group and had statistical significance (P=0.013). Conclusion Doxetaxel plus epirubiein regimen is effective for LABC with tolerable toxicity. Celeeoxib can enhance the effect and reduce the incidence of myalgia and arthralgia.
ABSTRACT
Objective Blocking the expression of Survivin with siRNA, and the effects of suppling the proliferation of PC-2 cell and inducing its apoptosis were investigated. Methods Constructed the siRNA against Survivin plasmid expression vector and transfected it into PC-2 cell with lipofectamineTM 2000, the changes of Survivin expression were detected by semi-quantitive RT-PCR and immunohistochemical method, The effect of suppressing the proliferation of PC-2 cell was detected by the method of MTT; the effect of inducing PC-2 cell apoptosis was detected by flow cytometry. Results The sequence specific siRNA can effectively block the expression of Survivin both at themRNA and protein levels, the expression inhibition ratio was 81.25% at mRNA level and 74. 24% at protein level;blocking the expression of Survivin can suppress the proliferation of PC-2 cell significantly, 24, 48 hours after the cell was reseeded, the proliferation inhibition ratio was 28. 00% and 33. 38% respectively; 24, 48 hours after the transfection, 8.46 % and 7.53 % cells were induced to apoptosis respectively. Conclusion The siRNA against Survivin plasmid expression vector constructed in the study can blocking the expression of Survivin in PC-2 cell effectively and specifically; blocking the expression of Survivin can signiilcantly suppress the proliferation of PC-2 cell and induce a certain degree cells apoptosis; RNAi against Survivin is of a certain value in the gene therapy of pancreatic cancer.
ABSTRACT
Objective We studied the expression of VEGF and its receptor,FLK－ 1,in neuroblastoma and its relation to clinical features.Methods With the help of antigen repairing,immunohistochemical analysis using antibody against VEGF,FLK－ 1 was carried out on speciments of 52 cases of neuroblastoma.Results There were 36 cases of VEGF and 34 cases of FLK－ 1 positive expression,the expression of them were nearly consistent.The positive rate of VEGF and FLK－ 1 were higher in metastatic tumors(28/34,26/34)than in non－ metastastic tumors and had statistical significance(respectively P<0.01,P<0.05).The expression of VEGF in UH tumors was higher than in FH tumors,and statistical value is significant(P<0.05).Conclusion VEGF is a vital angiogenic factor,and may play an improtant role in the progression and metastasis of neuroblastoma.Its expression and function correlates well to FLK－ 1,and may aid in predicting patients at risk of metastasis.