Objective To investigate the expression and their clinical significance of P?- glycoprotein (P?- gp), glutathione?- S?- transferase?- ?(GST?- ?)and DNA topoisomerase Ⅱ(TopoⅡ)in breast cancer. Methods The expressions of P?- gp, GST?- ? and TopoⅡ were detected in 60 cases of untreated primary breast cancer by using immunohistochemical S?- P method. Results The positive expression rates of P?- gp, GST?- ? and TopoⅡ in breast cancer were 37.1 %, 66.7 % and 55.0 % respectively. The expression of P?- gp and TopoⅡ had positive correlation with degree of differentiation(P

Objective To explore effects of paclitaxel on proliferation and migration of breast cancer Michigan Cancer Foundation-7 (MCF-7) cells via mammalian target of rapamycin (mTOR) signaling pathway.Methods The cases were randomly divided into four groups,including control group,paclitaxel low-dose group (0.25 μmol/L),paclitaxel medium-dose group (0.5 μmol/L),and paclitaxel high-dose group (1 μmol/L).The viability of MCF-7 cells was measured with methyl thiazolyl tetrazolium (MTT) assay.MCF-7 cell cycle was examined with flow cytometry.MCF-7 cell migration was tested with transwell migration assay.The levels of mTOR signalling pathway-related protein were assayed with Western blot.Results Compared to the control group,MCF-7 cell viability was significantly decreased in paclitaxel low,medium and high-dose groups (P ＜ 0.05),and the inhibitory rate was highest at 48 h (P ＜ 0.05).MCF-7 cell migration was significantly inhibited in paclitaxel low,medium and high-dose groups [(98 ± 9.78) vs (86.21 ± 6.58),(53.41 ± 3.16) and (42.00 ± 4.69),P ＜ 0.05].Moreover,compared to the control group,the number of MCF-7 cells at G1 phase was significantly increased in paclitaxel low,medium and high-dose groups [(52.14±6.13)％ vs (67.93 ±8.16)％,(72.32 ±3.67)％ and (78.53 ± 6.28)％,P ＜ 0.01],the number of MCF-7 cells at G2 phase was significantly reduced in paclitaxel low,medium and high-dose group [(13.68 ± 0.85) ％ vs (8.57 ± 1.03) ％,(5.30 ± 0.89) ％ and (3.46 ± 0.78) ％,P ＜0.01].The phosphorylations of 4E binding protein (4EBP1) and mTOR proteins as well as the expressions of cell-cycle protein D1 (Cyclin D1) and matrix metalloproteinase-9 (MMP-9) were significantly inhibited in paclitaxel low,medium and high-dose groups (P ＜ 0.01).Conclusions These results suggested paclitaxel could inhibit proliferation and migration in breast cancer MCF-7 cells,which might be related to mTOR signal pathway.

[Objective] To investigate the variation of Q promoter (Qp) in nasopharyngeal carcinoma (NPC) cells, and to compare the existing two mutant sites [62 225 site(g→a)and 62 422 site (g→c) ] Qp in NPC cells with the Qp in B95.8 cell line in the functional and biological difference. [Methods] The Qp sequence was amplified in the samples from 29 cases of paraffin-embedded tissues of NPC suffers and 14 cases of peripheral blood of healthy adults by polymerase chain reaction (PCR) method (totally 43 cases). The point mutations on specified sites were analyzed and statistically compared from sequencing results. The sequences of variant and prototype Qp were amplified by PCR and cloned into luciferase reporter vector (pGL3-basic), then transfected into HaCat cells respectively. The transcriptional activity was compared between variant and prototype Qp using luciferase reporter system. The DNA binding affinity of mutant and prototype Qp to Sp1 was compared through chromatin immunoprecipitation (CHIP) method since mutation of nt 62 225 located in a Spl binding site. [Results] The mutation rate of Qp was significantly higher in NPC compared with healthy controls (P=0.039 5, <0.05), which suggested the variant Qp was closely associated with NPC. The transcription of the luciferase gene promoted by variant Qp was significant more than that of prototype Qp in transient transfection assay (2.5:1, P<0.05). The binding affinity of variant Qp to Sp1 was about 1.52 times higher than that of prototype Qp as determined by quantitative ChIP assay. [Conclusions] The transcriptional activity was enhanced in variant Qp in NPC cells compared with prototype, which possibly through the higher binding affinity to Sp1. We suggest that the mutated Qp may play an important role during the EBV infection and transformation of nasopharyngeal epithelium.

【Objective】 To identify and propose blood transfusion suggestions for 3 children suspected to have red blood cell T polyagglutination. 【Methods】 According to the RBC reactions with phytohemagglutinin, adult serum and cord blood serum, aggregation test with polybrene reagent and MN antigen phenotype test were carried out on 3 children to confirm the presence of T polyagglutination. The donor serum with negative or weak reactions was selected by minor cross matching for the 3 children who needed therapeutic plasma exchange(TPE). 【Results】 Three cases of RBC T polyagglutination were caused by bacterial infection, with transient appearance of MN antigen; the samples were reactive to peanut agglutinin, soybean agglutinin, adult serum but nonreactive to cord blood serum, and didn′t aggregate after adding polybrene reagent. After receiving timely TPE, the T polyagglutination gradually disappeared. 【Conclusion】 Some bacteria, such as Streptococcus pneumoniae, may cause polyagglutination of red blood cells. The patients with suspected T polyagglutination should be diagnosed in time. For T polyagglutination patients, the minor matched plasma should be used for avoiding the random plasma with anti-T antibody transfusion.