Objectives:1. Establishing mice model of breast cancer by giving MCF-7, MCF-7 C and MCF-7 H cancer cells.2. Comparing the antitumor effects of DCIK and DCIK-H cells in breast cancer amongst MCF-7, MCF-7 C and MCF-7 Hers2 mice groups.3. Comparing the proliferation rate after the intervention of DCIK and DCIK-H cells amongst MCF-7, MCF-7 C and MCF-7 Hers2 mice groups by analyzing Ki-67 expression.Methods:1. In vitro culture of MCF-7, MCF-7 C and MCF-7 H breast cancer cell strain.2. In vitro culture of DCIK and DCIK-H cells.3. Establishing mice model of MCF-7, MCF-7 C and MCF-7 H breast cancer by using Balb/c nude mice.4. DCIK, DCIK-H cells and serum-free medium are injected respectively to MCF-7, MCF-7 C and MCF-7 Hers2 mice creating DCIK group, DCIK-H group and Control group.5. Analyzing the difference of Ki-67 expression by using immunochemistry staining after the intervention of DCIK and DCIK-H cells amongst-7, MCF-7 C and MCF-7 Hers2 mice groups.Results:1. Successful establishment of MCF-7, MCF-7 C and MCF-7 H breast cancer mice model.2. Significant difference in tumor size of MCF-7, MCF-7 C and MCF-7 H mice groups before and after the intervention of DCIK and DCIK-H cells in which smaller tumor size is found in DCIK and DCIK-H intervention groups but bigger size in control group.3. Difference of Ki-67 expression also found in breast cancer mice models before and after DCIK and DCIK-H intervention which showing a downward trend.Conclusions:1. DCIK cells and DCIK-H cell could cause smaller tumor size in MCF-7, MCF-7 C and MCF-7 H breast cancer mice model where the anti tumor effect of DCIK-H group is better than DCIK group.2. We found that Ki-67 expression is declining after the intervention of DCIK and DCIK-H cells. |