Breast cancer refers to a malignant tumor that occurs in the epithelial tissue of the breast gland. Among them, female patients accounted for 99%, males only accounted for 1%, and female cancer mortality ranked second. Most breast cancers are hormone-dependent tumors, and ER-positive breast cancer accounts for about 60-75% of all breast cancers, of which about 65% are PR-positive. Among them, about 10.0% to 20.8% of patients had negative ER, PR and Her-2, which is triple negative breast cancer. Triple-negative breast cancer is the most important factor in the study of breast cancer because of its special biological behavior and clinical pathological features, and its rapid development and poor prognosis. So how many types of breast cancer, how to choose the right model in the research process?
1. Which cell model do I need? Is it easy to operate?
Although a variety of cell lines are available for reference, during the study, the commonly used cell line was MDA-MB-231 for triple-negative breast cancer, and the cell line commonly used for non-negative was MCF-7. As the best tool for in vitro studies, lentivirus also has a good infection effect in breast cancer cell lines.
*More comprehensive pre-experiment information, please consult the local salesman
Second, the cell experiment works well, how does the animal experiment do?
In vivo research is required for high score articles. MCF-7 and MDA-MB-231 are cell lines commonly used in breast cancer xenograft studies. Today, I will introduce two common models of breast cancer research in vivo: 1) left ventricular injection simulated metastasis model; 2) fat pad implantation in situ tumor formation model.
Second, the in vitro and in vivo models have been selected, then what kind of lentiviral vector does my experiment need to use to manipulate the gene?
Promoters, fluorescent markers, and resistance tags are the three major factors we need to consider when choosing a carrier. Different components also require corresponding changes in the experiment. For breast cancer research, MGA is a more common breast tumor tissue-specific promoter. According to the example of a god figure, customizing your exclusive carrier is as simple as that! 
Shanghai Jikai Gene Chemical Technology Co., Ltd. was established in 2002 and has a BSL-2 level lentivirus packaging laboratory. The virus production line has passed the ISO9001 quality management system verification, and the monthly average custom genetic virus product packaging has exceeded 1000 times. Lentiviral production uses six QC assays, viral purity fractionation and absolute quantitative detection of viral titers to ensure virus quality.
400 dedicated Jikai people, use professional to change your efficiency.
PS: Friends who want to know more about the Tumor Tools Guide can pay attention to the "Jikai Gene" WeChat public number, and more exciting articles waiting for you.
references
[1] Neve, Richard M., et al. "A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes." Cancer cell 10.6 (2006): 515-527.
[2] Yang, L., et al. "FZD7 has a critical role in cell proliferation in triple negative breast cancer." Oncogene 30.43 (2011): 4437-4446.
[3] Wei, Yingze, et al. “PAâ€MSHA inhibits the growth of doxorubicin-resistant MCFâ€7/ADR human breast cancer cells by downregulating Nrf2/p62.†Cancer Medicine 5.12 (2016): 3520-3531.
[4] Hou, Jinling, et al. "Genomic amplification and a role in drug-resistance for the KDM5A histone demethylase in breast cancer." American journal of translational research 4.3 (2012): 247.
[5] Xu, Yue-Mei, et al. "HRD1 suppresses the growth and metastasis of breast cancer cells by promoting IGF-1R degradation." Oncotarget 6.40 (2015): 42854.
[6]Ren, Yong-qiang, Fengkui Fu, and Jianjun Han. "MiR-27a modulates radiosensitivity of triple-negative breast cancer (TNBC) cells by targeting CDC27." Medical science monitor: international medical journal of experimental and clinical research 21 (2015): 1297.
[7] Lv, Zhiâ€Dong, et al. "Silencing of Prrx1b suppresses cellular proliferation, migration, invasion and epithelial-mesenchymal transition in triple-negative breast cancer." Journal of cellular and molecular medicine (2016).
[8]Yue, LU, et al. "Relationship Between HSP70 and ERBB2 Expression in Breast Cancer Cell Lines Regarding Drug Resistance." Anticancer research 36.3 (2016): 1243-1249.
[9] Cai, Xiaopeng, et al. "Survivin regulates the expression of VEGF-C in lymphatic metastasis of breast cancer." Diagnostic pathology 7.1 (2012): 1.
[10] Bartucci, M., et al. "TAZ is required for metastatic activity and chemoresistance of breast cancer stem cells." Oncogene 34.6 (2015): 681-690.
In the previous issues, I have shared a summary of the in vitro and in vivo models and tools of several large cancer species. If you want to see it again, please post the following:
1. Review of in vitro and in vivo models of lung cancer research
2. Review of in vitro and in vivo models of colorectal cancer research
3. Overview of in vivo and in vitro models of gastric cancer research
4. Summary of in vitro and in vivo models of liver cancer
5. Summary of in vitro and in vivo models of pancreatic cancer research
6. Overview of internal and external models of hematological tumor research
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