scholarly journals It May Be Possible to Prevent both Early and Late Relapses in Breast Cancer; Perhaps This Is an Opportunity for Sensors or Biosensors to Help

Sensors ◽  
2020 ◽  
Vol 20 (24) ◽  
pp. 7261
Author(s):  
Michael Retsky

Data presented in 1993 showed an unexpected bimodal relapse pattern in surgically treated breast cancer [...]

2009 ◽  
Vol 49 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Annika Malmström ◽  
Jörgen Hansen ◽  
Lena Malmberg ◽  
Lena Carlsson ◽  
Jan-Henry Svensson ◽  
...  

1991 ◽  
Vol 3 (4) ◽  
pp. 267-270 ◽  
Author(s):  
G. Spinelli ◽  
N. Bardazzi ◽  
A. Citernesi ◽  
M. Fontanarosa ◽  
P. Curiel

2012 ◽  
Vol 53 ◽  
pp. S119-S120
Author(s):  
A.S. Fernandes⁎ ◽  
M. Cipriano ◽  
J. Costa ◽  
M.F. Cabral ◽  
J. Miranda ◽  
...  

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Yike Wang ◽  
Lifeng Dong ◽  
Fang Wan ◽  
Fangfang Chen ◽  
Dianlei Liu ◽  
...  

AbstractThis study explored the role of MTDH in regulating the sensitivity of breast cancer cell lines to gemcitabine (Gem) and the potential miRNAs targeting MTDH. The expression of MTDH in cancer tissues and cells was detected by immunohistochemical staining or qRT-PCR. The target genes for MTDH were predicted by bioinformatics and further confirmed by dual-luciferase reporter assay and qRT-PCR. Cancer cells were transfected with siMTDH, MTDH, miR-9-3p inhibitor, or mimics and treated by Gem, then CCK-8, colony formation assay, tube formation assay, flow cytometry, wound healing assay, and Transwell were performed to explore the effects of MTDH, miR-9-3p, and Gem on cancer cell growth, apoptosis, migration, and invasion. Expressions of VEGF, p53, cleaved caspase-3, MMP-2, MMP-9, E-Cadherin, N-Cadherin, and Vimentin were determined by Western blot. MTDH was high-expressed in cancer tissues and cells, and the cells with high-expressed MTDH were less sensitive to Gem, while silencing MTDH expression significantly promoted the effect of Gem on inducing apoptosis, inhibiting cell migration, invasion, and growth, and on regulating protein expressions of cancer cells. Moreover, miR-9-3p had a targeted binding relationship with MTDH, and overexpressed miR-9-3p greatly promoted the toxic effects of Gem on cancer cells and expressions of apoptosis-related proteins, whereas overexpressed MTDH partially reversed such effects of overexpressed miR-9-3p. The study proved that miR-9-3p regulates biological functions, drug resistance, and the growth of Gem-treated breast cancer cells through targeting MTDH.


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