目的探讨超声弹性成像(Ultrasonic Elastography,UE)联合乳腺影像报告和数据系统(Breast Imaging Reporting And Data System,BI-RADS)在鉴别小乳腺癌与乳腺增生中的应用价值。方法选取2016年6月至2018年6月本院小乳腺癌、乳腺增生患者...目的探讨超声弹性成像(Ultrasonic Elastography,UE)联合乳腺影像报告和数据系统(Breast Imaging Reporting And Data System,BI-RADS)在鉴别小乳腺癌与乳腺增生中的应用价值。方法选取2016年6月至2018年6月本院小乳腺癌、乳腺增生患者各100例,所有患者均给予常规超声、UE检查,分析所有患者UE、BI-RADS情况及UE联合BI-RADS对小乳腺癌与乳腺增生的鉴别价值。结果小乳腺癌患者UE、BI-RADS评分明显高于乳腺增生患者,有统计学差异(P<0.05);在鉴别小乳腺癌与乳腺增生的敏感度、特异度、准确度中,BI-RADS为86.00%、84.00%、85.00%,UE为80.00%、82.00%、81.00%,UE联合BI-RADS为96.00%、94.00%、95.00%,UE联合BI-RADS显著高于UE、BI-RADS(P<0.05)。结论UE、BI-RADS可作为鉴别小乳腺癌与乳腺增生的重要方法,且UE联合BI-RADS的鉴别效能更高,值得临床推广。展开更多
Background Overexpression of breast cancer-specific gene 1 （SNCG） is associated with poor prognosis in advanced breast cancer patients. This study aimed to determine the effects of SNCG knockdown in breast cancer ce...Background Overexpression of breast cancer-specific gene 1 （SNCG） is associated with poor prognosis in advanced breast cancer patients. This study aimed to determine the effects of SNCG knockdown in breast cancer cells by using small hairpin RNA （shRNA）.Methods Four different SNCG shRNA oligonucleotides were designed and chemically synthesized to construct mammalian expression vectors. These vectors were then stably transfected into a breast cancer MCF-7 cell line to knockdown SNCG expression. After SNCG knockdown was confirmed, the stable cell lines were inoculated into nude mice. SNCG mRNA and protein expressions were analyzed by semi-quantitative reverse transcription-polymerase chain reaction （RT-PCR） and immunohistochemistry, respectively in both the stable cell lines and xenografts.Results All four SNCG shRNA constructs significantly reduced SNCG mRNA and protein levels in MCF-7 cells, as compared to the unrelated sequence control shRNA and the liposome control mice （P〈0.05）. SNCG-knockdown MCF-7cells formed significantly smaller tumor masses than cells expressing the unrelated sequence control or the liposome control mice （P〈0.05）.Conclusion SNCG shRNA effectively suppressed breast cancer cell formation in vivo and may be a useful clinical strategy to control breast cancer展开更多
Background Signal transducer and activator of transcription 3 （STAT3） is usually constitutively activated in a variety of malignancies. It directly contributes to tumorigenesis, invasion, and metastasis. The surgica...Background Signal transducer and activator of transcription 3 （STAT3） is usually constitutively activated in a variety of malignancies. It directly contributes to tumorigenesis, invasion, and metastasis. The surgical treatment of breast cancer has made no breakthroughs in terms of treatment effect, in spite of its long history. Current biotherapies bring a note of optimism to breast cancer treatment. To explore the possibility of a siRNA targeted STAT3 blocking treatment for over-activated tumor cells, we evaluated the efficacy of a STAT3 siRNA on human breast cancer cells in vitro and in vivo. Methods Three MCF-7 human breast cancer cell lines were tested： control MCF-7 cells, non-specific siRNA transfected MCF-7 cells and STAT3 siRNA transfected MCF-7 cells. Expression of STAT3 in MCF-7 cells was inhibited by RNA interference （RNAi）. The STAT3 mRNA and protein levels were detected by semi-quantity RT-PCR and Western blotting. Cell proliferation and apoptosis were determined by MTT method and flow cytometry. The three groups of MCF-7 cells mentioned above were transplanted subcutanuously into nude mice and their tumorgenic ability observed. The STAT3 mRNA and protein levels of the samples from tumors in different groups were determined by semi-quantity RT-PCR and Western blotting and compared. Results In STAT3 siRNA transfected MCF-7 cells, the expressions （STAT3/13-actin） of STAT3 mRNA （0.327±0.020） and protein （0.153±0.006） were significantly lower than that in control MCF-7 cells （mRNA 1.093±0.018, protein 1.374±0.022） and non-specific siRNA transfected MCF-7 cells （mRNA 1.035_±0.050, protein 1.320±0.033） （P 〈0.05）. MTT showed that cell proliferation was significantly reduced and the cell growth inhibition ratio in the STAT3-siRNA group was （44.00±5.10）%, significantly higher than that in non-specific siRNA transfected MCF-7 cells （（16.10_±1.05）%, P 〈0.05）. Flow cytometry results showed that more apoptosis was observed in the STAT3-siRNA group. The rat展开更多
文摘目的探讨超声弹性成像(Ultrasonic Elastography,UE)联合乳腺影像报告和数据系统(Breast Imaging Reporting And Data System,BI-RADS)在鉴别小乳腺癌与乳腺增生中的应用价值。方法选取2016年6月至2018年6月本院小乳腺癌、乳腺增生患者各100例,所有患者均给予常规超声、UE检查,分析所有患者UE、BI-RADS情况及UE联合BI-RADS对小乳腺癌与乳腺增生的鉴别价值。结果小乳腺癌患者UE、BI-RADS评分明显高于乳腺增生患者,有统计学差异(P<0.05);在鉴别小乳腺癌与乳腺增生的敏感度、特异度、准确度中,BI-RADS为86.00%、84.00%、85.00%,UE为80.00%、82.00%、81.00%,UE联合BI-RADS为96.00%、94.00%、95.00%,UE联合BI-RADS显著高于UE、BI-RADS(P<0.05)。结论UE、BI-RADS可作为鉴别小乳腺癌与乳腺增生的重要方法,且UE联合BI-RADS的鉴别效能更高,值得临床推广。
文摘Background Overexpression of breast cancer-specific gene 1 （SNCG） is associated with poor prognosis in advanced breast cancer patients. This study aimed to determine the effects of SNCG knockdown in breast cancer cells by using small hairpin RNA （shRNA）.Methods Four different SNCG shRNA oligonucleotides were designed and chemically synthesized to construct mammalian expression vectors. These vectors were then stably transfected into a breast cancer MCF-7 cell line to knockdown SNCG expression. After SNCG knockdown was confirmed, the stable cell lines were inoculated into nude mice. SNCG mRNA and protein expressions were analyzed by semi-quantitative reverse transcription-polymerase chain reaction （RT-PCR） and immunohistochemistry, respectively in both the stable cell lines and xenografts.Results All four SNCG shRNA constructs significantly reduced SNCG mRNA and protein levels in MCF-7 cells, as compared to the unrelated sequence control shRNA and the liposome control mice （P〈0.05）. SNCG-knockdown MCF-7cells formed significantly smaller tumor masses than cells expressing the unrelated sequence control or the liposome control mice （P〈0.05）.Conclusion SNCG shRNA effectively suppressed breast cancer cell formation in vivo and may be a useful clinical strategy to control breast cancer
文摘Background Signal transducer and activator of transcription 3 （STAT3） is usually constitutively activated in a variety of malignancies. It directly contributes to tumorigenesis, invasion, and metastasis. The surgical treatment of breast cancer has made no breakthroughs in terms of treatment effect, in spite of its long history. Current biotherapies bring a note of optimism to breast cancer treatment. To explore the possibility of a siRNA targeted STAT3 blocking treatment for over-activated tumor cells, we evaluated the efficacy of a STAT3 siRNA on human breast cancer cells in vitro and in vivo. Methods Three MCF-7 human breast cancer cell lines were tested： control MCF-7 cells, non-specific siRNA transfected MCF-7 cells and STAT3 siRNA transfected MCF-7 cells. Expression of STAT3 in MCF-7 cells was inhibited by RNA interference （RNAi）. The STAT3 mRNA and protein levels were detected by semi-quantity RT-PCR and Western blotting. Cell proliferation and apoptosis were determined by MTT method and flow cytometry. The three groups of MCF-7 cells mentioned above were transplanted subcutanuously into nude mice and their tumorgenic ability observed. The STAT3 mRNA and protein levels of the samples from tumors in different groups were determined by semi-quantity RT-PCR and Western blotting and compared. Results In STAT3 siRNA transfected MCF-7 cells, the expressions （STAT3/13-actin） of STAT3 mRNA （0.327±0.020） and protein （0.153±0.006） were significantly lower than that in control MCF-7 cells （mRNA 1.093±0.018, protein 1.374±0.022） and non-specific siRNA transfected MCF-7 cells （mRNA 1.035_±0.050, protein 1.320±0.033） （P 〈0.05）. MTT showed that cell proliferation was significantly reduced and the cell growth inhibition ratio in the STAT3-siRNA group was （44.00±5.10）%, significantly higher than that in non-specific siRNA transfected MCF-7 cells （（16.10_±1.05）%, P 〈0.05）. Flow cytometry results showed that more apoptosis was observed in the STAT3-siRNA group. The rat
