AIM: To evaluate the influence of radiofrequency (RF) hyperthermia on immunity function in mice. METHODS: The expression pattern of T helper type 1 (Th1) and T helper type 2 (Th2) cytokines in splenocyte culture supernatants, mainly the expression levels of IFN-?, IL-2, IL-4 and IL-10 in splenocyte culture supernatants of mice in tumor-bearing group, surgical resection group, RF therapy group and normal control group were detected by enzyme-linked immunoadsordent assay (ELISA). RESULTS: IL-2 concentration in two weeks after RF therapy group was higher than that in two weeks after surgical resection and normal control groups (P0.05). CONCLUSION: RF hyperthermia may activate the transformation from Th2 to Th1 and facilitate the excretion of Th1 type cytokines that play an important role in the anti-tumor immunity.

AIM: To evaluate the relationship between uPA and NF-?B p65 expression and its clinical significance in breast cancer. METHODS: The uPA mRNA was measured by real-time fluorescent quantitative PCR in 46 cases of breast cancer tissues and their adjacent counterparts. NF-?B p65 were measured using immunohistochemistry. RESULTS: The expression of uPA gene was elevated in 63% of cases, and there was a strong correlation between NF-?B p65 and uPA expression (r=0.451,P

AIM:To observe the effect on NF-?B pathway and cell motility in breast cancer cell lines after transfection of dominant negative I?B? plasmid.METHODS:After stable transfection of mutant I?B? plasmid into highly metastatic breast cancer lines MDA-MB-231 and MDA-MB-435,we detected NF-?B binding activity by EMSA,cell growth ability by cell growth curve,colony forming test,and cell motility by millicell-PCF chamber.RESULTS:Constitutive activities in MDA-MB-231 and MDA-MB-435 were observed.Stable transfection of a dominant negative Ⅰ?B? resulted in downregulation of NF-?B binding activity,thus inhibited cell mobility without significant effect on cell growth.CONCLUSION:Cell migration ability is inhibited in highly invasive breast cancer cells by inhibition of NF-?B pathway in vitro.

AIM: To investigate the role of nuclear factor ?B (NF-?B) in the induction of IL-8 gene by TNF-? in colon cancer cells and the effect of antioxidant on the induction of IL-8. METHODS: ELISA was used to detect the concentrations of IL-8. IL-8 mRNA was analyzed by using RT-PCR. NF-?B in the cell nuclei was detected with electrophoretic mobility shift assay. RESULTS: (1) IL-8 production and IL-8 mRNA expression induced by TNF-? was blocked by pyrrolidine dithiocarbamate (PDTC). (2) TNF-? triggered the activation and translocation of NF-?B and PDTC inhibited the activation of NF-?B induced by TNF-?. CONCLUSION: The induction of IL-8 gene and protein by TNF-? is dependent on the activation of NF-?B. Antioxidants may inhibit the induction of IL-8 gene and protein through inhibiting NF-?B activation.