scholarly journals JAK3 inhibitor VI is a mutant specific inhibitor for epidermal growth factor receptor with the gatekeeper mutation T790M

2015 ◽  
Vol 6 (4) ◽  
pp. 409 ◽  
Author(s):  
Naoyuki Nishiya
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Specific Inhibitor ◽  
Epidermal Growth ◽  
Jak3 Inhibitor

A specific inhibitor of the epidermal growth factor receptor tyrosine kinase

Science ◽  
1994 ◽  
Vol 265 (5175) ◽  
pp. 1093-1095 ◽  
Author(s):  
D. Fry ◽  
A. Kraker ◽  
A McMichael ◽  
L. Ambroso ◽  
J. Nelson ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Growth Factor Receptor ◽  
Specific Inhibitor ◽  
Epidermal Growth

scholarly journals BE-23372M, a Novel and Specific Inhibitor for Epidermal Growth Factor Receptor Kinase

1994 ◽  
Vol 85 (3) ◽  
pp. 253-259 ◽  
Author(s):  
Seiichi Tanaka ◽  
Takayoshi Okabe ◽  
Shinya Chieda ◽  
Kaori Endo ◽  
Tomoko Kanoh ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Specific Inhibitor ◽  
Receptor Kinase ◽  
Epidermal Growth

Effects of the administration of epidermal growth factor receptor specific inhibitor cetuximab, alone and in combination with cisplatin, on proliferation and apoptosis of Hep-2 laryngeal cancer cells

2014 ◽  
Vol 128 (10) ◽  
pp. 902-908 ◽  
Author(s):  
F Bussu ◽  
G Pozzoli ◽  
V Giglia ◽  
D Rizzo ◽  
A Limongelli ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Cancer ◽  
Growth Factor Receptor ◽  
Specific Inhibitor ◽  
Clinical Effectiveness ◽  
Inhibition Of Proliferation ◽  
Proliferation And Apoptosis ◽  
Epidermal Growth

AbstractBackground:Epidermal growth factor receptor (EGFR) overexpression and prognostic value in head and neck squamous cell cancer is the basis for targeting by anti-EGFR antibodies, which increase the efficacy of radiotherapy. In order to evaluate the best therapeutic schedule, the effects of cetuximab (C225) on Hep-2 cell proliferation, alone and in combination with cisplatin, were studied.Methods:Hep-2 cells were treated with cetuximab alone or in combination with cisplatin. After determining cell viability with trypan blue, morphological features of apoptotic degeneration were analysed by fluorescence microscopy with Hoechst 33258 stain.Results:Cetuximab alone mildly inhibited Hep-2 proliferation and showed no pro-apoptotic effects. When administered concomitantly with cisplatin, cetuximab synergistically increased inhibition of proliferation and apoptosis.Conclusion:The antiproliferative activity of cetuximab is consistent with its hypothesised role in inhibiting repopulation. However, the increase in the effects of pro-apoptotic agents induced by cetuximab may be even more relevant to its clinical effectiveness than the inhibition of repopulation.

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