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Objective@#To explore the feasibility of 7, 12-dimethylbenz[a] anthracene (DMBA) induced tree shrew breast cancer model, and compare the effects of two administration modes by gavage and mammary gland injection.@*Methods@#A total of 40 tree shrews were randomly divided into two groups (20 animals per group): DMBA gavage group and mammary gland injection group. DMBA was dissolved in edible vegetable oil. For gavage group, tree shrews were administered with DMBA solutions (15 mg/kg) by gavage once a day. For mammary gland injection group, DMBA solution (10 mg/kg) was injected into the mammary fat pad of tree shrews, and the injection was performed for a total of 3 times. From the first administration of DMBA, medroxyprogesterone acetate (MPA, 100 mg/kg) was intramuscularly injected into the muscles of the lateral thighs of tree shrews at the same time, for a total of 5 times. The tumorigenesis and survival of tree shrews were monitored. The tumor histological morphology was observed by HE staining. The expression of estrogen receptor (ER), progesterone receptor (PR), cytokeratin5/6 (CK5/6) and human epidermal factor receptor-2 (HER-2) was detected by immunohistochemical staining.@*Results@#In the gavage group, there were 10 deaths, and 4 tree shrews developed mammary tumors with 20.0% (4/20) tumor formation rate. The success rate of mammary cancer modeling was 10.0% (2/20), and the tumor formation time was 197.3±15.1 days. In the mammary gland injection group, there were 8 tree shrews died, and 9 tree shrews formed tumors with 45.0% (9/20) tumor formation rate. The success rate of mammary cancer modeling was 40.0% (8/20), and the tumor formation time was 71.8±19.0 days. There was no significant difference in mortality and tumor formation rate (P>0.05) between the two groups (all P>0.05). However, in the mammary gland injection group, the success rate of mammary cancer modeling was significantly higher than that in the gavage group (P<0.05), whereas the tumor formation time was markedly shorter than that in the gavage group (P<0.01). The pathological types in the gavage group included ductal hyperplasia, intraductal papilloma and ductal carcinoma in situ, while those in the breast injection group included intraductal papilloma and ductal carcinoma in situ. In both groups, immunohistochemical staining showed the negative expression of HER-2 but positive expression of ER, PR and CK5/6 with varying degrees.@*Conclusion@#Both the DMBA gavage and mammary gland injection can successfully establish the tree shrew breast cancer model, and the modeling effect of mammary gland injection is better than gavage.
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Background and purpose: Factor that binds to the inducer of short transcripts of human immuno-deficiency virus-1 (FBI-1) in a variety of malignant tumors showed high expression levels, which may be closely related to tumor proliferation and differentiation, angiogenesis, metastasis, but its relationship with breast cancer has not been fully elucidated. The purpose of this study was to investigate the expression of FBI-1 in breast cancer cells, and to study the effect of FBI-1 gene expression on the proliferation of breast cancer cells and its possible mechanism. Methods:Real-time fluorescent quantitative polymerase chain reaction (RTFQ-PCR) and Western blot analysis were applied to detect FBI-1 expression in normal human mammary epithelial cell line MCF-10A and breast cancer cell MCF-7. RNA interference method was used to down-regulate FBI-1 expression in MCF-7 cells. The cell proliferation was measured by CCK-8 kit and colony formation assay. RTFQ-PCR and Western blot were used to detect the expression of FBI-1 and NF-κBp65 in MCF-7 cells before and after the interference of FBI-1 expression. Results: The expression of FBI-1 was higher in breast cancer cells than that in normal human mammary epithelial cells (P<0.05). The effects of FBI-1 down-regulation inhibited proliferation in MCF-7 cells (P<0.05). At the same time, after inhibition of FBI-1, the NF-κBp65 mRNA and protein expression levels were significantly decreased (P<0.05). Conclusion: FBI-1 is highly expressed in breast cancer cells. Down-regulated FBI-1 expression can inhibit the proliferation of breast cancer cells,and its mechanism may be related to the inhibition of NF-κB signaling pathway.
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Objective To explore the effects and mechanism of triptolide on proliferation and apoptosis of breast cancer MCF-7 cells.Methods MCF-7 cells were treated by different concentrations of triptolide.CCK-8 as-say was employed to detect the cell proliferation. The morphological changes were observed by an inverted micro-scope.The apoptosis rate was detected by flow cytometry.Expressions of Bcl-2,Bax,Survivin and Caspase-3 were measured by qRT-PCR and Western blot. Results Triptolide inhibited the proliferation of MCF-7 cells in a dose and time-dependent manner at a suitable range.Triptolide induced morphological changes and apoptosis.Triptolide also down-regulated Bcl-2 and Survivin expressions and up-regulated Bax and Caspase-3 expressions. Conclu-sions Triptolide inhibits proliferation and induces apoptosis of MCF-7 cells,and its mechanism may be related to down-regulation of Bcl-2 and Survivin expressions and up-regulation of Bax and Caspase-3 expressions.
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Objective To probe the effect of perioperative therapeutic regime on breast reconstruction after surgery in breast cancer patients.Methods We retrospectively reviewed the clinical data of 145 consecutive breast cancer patients with 162 reconstructions.Results 127 of 145 patients got an excellent or good appearance (87.6％),and 42 cases had complications occurring in 162 operations (25.9％).After a median follow-up of 38.4 months,recurrences were found in 9 patients,3 cases died,and the disease free survival rate was 93.1％.Multivariate analysis showed that radiation therapy,without nipple-sparing and one-stage prosthesis implant were independent risk factors for negative postoperative aesthetic outcome;Delayed reconstruction and implant reconstruction were found to be protective factors for the postoperative complications.Conclusions Although the survival rate appears to be scarcely affected,different treatment modalities in reconstruction strategy bring different clinical results and outcomes.The perioperative decision-making of reconstruction strategy should be based on oncological safety,postoperative complications,aesthetic outcomes and subsequent therapies.
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<p><b>BACKGROUND</b>This study was designed in an attempt to determine the influence of neoadjuvant chemotherapy on estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (Her-2), and Ki-67 expressions in patients with breast cancer.</p><p><b>METHODS</b>Pre- and post-neoadjuvant chemotherapy, paired-tumor specimens from 103 patients with breast cancer administrated with anthracycline or anthracycline combined taxane regimen were collected. Immunohistochemical staining for ER, PR, Her-2, and Ki-67 was performed by the DAKO EnVision method.</p><p><b>RESULTS</b>Among the 103 cases, five patients (4.9%) had a complete response (CR), 82 (79.6%) partial response (PR), 15 (14.6%) stable disease (SD), and one (0.9%) progressive disease (PD), yielding an overall response rate (CR + PR) of 84.5%. Nine patients achieved pathological CR. There was a significant decrease in the average index of Ki-67 postneoadjuvant chemotherapy, compared with that before chemotherapy (24.1% vs. 39.7%, P < 0.001). After neoadjuvant chemotherapy, the changes of Ki-67 in different subtypes of breast cancer were different (P < 0.001), and these changes correlated with response to neoadjuvant chemotherapy (P < 0.001). No significant changes in immunohistochemical expression were observed for ER, PR and Her-2.</p><p><b>CONCLUSIONS</b>Neoadjuvant chemotherapy apparently reduced Ki-67 index in primary breast carcinomas, but profiles for ER, PR and Her-2 were not significantly different before and after neoadjuvant chemotherapy. The change of Ki-67 correlated with molecular subtypes and response to neoadjuvant chemotherapy, suggesting that Ki-67 index was a surrogate marker to predict the treatment response of neoadjuvant chemotherapy.</p>