scholarly journals The use of matrigel has no influence on tumor development or PET imaging in FaDu human head and neck cancer xenografts

2016 ◽  
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Frederikke P. Fliedner ◽  
Anders E. Hansen ◽  
Jesper T. Jørgensen ◽  
Andreas Kjær
Chemotherapy ◽  
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Sreenivasulu Chintala ◽  
Károly Tóth ◽  
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...  

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Jens Sörensen ◽  
Mikael Karlsson ◽  
Ingela Turesson ◽  
Bengt Langström ◽  
...  

2019 ◽  
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Dong-Hoon Won ◽  
Shin Hye Chung ◽  
Ji-Ae Shin ◽  
Kyoung-Ok Hong ◽  
In-Hyoung Yang ◽  
...  

1995 ◽  
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T. P. J. Mulder ◽  
J. J. Manni ◽  
H. M. J. Roelofs ◽  
W. H. M. Peters ◽  
A. Wiersma

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Kristin Gurtner ◽  
Mechthild Krause ◽  
...  

2009 ◽  
Vol 2009 ◽  
pp. 1-10 ◽  
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Arlene D. Parsons ◽  
Katherine A. Foster ◽  
Kevin P. Orcutt ◽  
Melissa A. Fath ◽  
...  

The hypothesis that the Akt inhibitor, perifosine (PER), combined with inhibitors of glutathione (GSH) and thioredoxin (Trx) metabolism will induce cytotoxicity via metabolic oxidative stress in human head and neck cancer (HNSCC) cells was tested. PER induced increases in glutathione disulfide (%GSSG) in FaDu, Cal-27, and SCC-25 HNSCCs as well as causing significant clonogenic cell killing in FaDu and Cal-27, which was suppressed by simultaneous treatment with N-acetylcysteine (NAC). An inhibitor of GSH synthesis, buthionine sulfoximine (BSO), sensitized Cal-27 and SCC-25 cells to PER-induced clonogenic killing as well as decreased total GSH and increased %GSSG. Additionally, inhibition of thioredoxin reductase activity (TrxRed) with auranofin (AUR) was able to induce PER sensitization in SCC-25 cells that were initially refractory to PER. These results support the conclusion that PER induces oxidative stress and clonogenic killing in HNSCC cells that is enhanced with inhibitors of GSH and Trx metabolism.


2019 ◽  
Vol 49 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Szu‐Chin Li ◽  
Ching‐Chih Lee ◽  
Chin‐Mu Hsu ◽  
Hsien‐Bin Huang ◽  
Yu‐Chieh Su

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