Abstract 2239: The effect combining the KIT inhibitor Imatinib with the PI3K inhibitor BKM120 or the dual PI3K/mTOR inhibitor BEZ235 on the proliferation of gastrointestinal stromal tumor cell lines

Author(s):  
Fang Li ◽  
Joseph Growney ◽  
Linda Battalagine ◽  
Shumei Qiu ◽  
Paul Manley ◽  
...  
Author(s):  
Kazuhiro Noma ◽  
Yoshio Naomoto ◽  
Mehmet Gunduz ◽  
Junji Matsuoka ◽  
Tomoki Yamatsuji ◽  
...  

Oncotarget ◽  
2019 ◽  
Vol 10 (19) ◽  
pp. 1798-1811 ◽  
Author(s):  
Pierre Vandenberghe ◽  
Marine Delvaux ◽  
Perrine Hagué ◽  
Christophe Erneux ◽  
Jean-Marie Vanderwinden

2016 ◽  
Vol 31 (8) ◽  
pp. 302-310 ◽  
Author(s):  
Achim Paulmichl ◽  
Dominik Summer ◽  
Claudia Manzl ◽  
Christine Rangger ◽  
Francesca Orlandi ◽  
...  

Pharmacology ◽  
2006 ◽  
Vol 77 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Hans Prenen ◽  
Gunther Guetens ◽  
Gert de Boeck ◽  
Maria Debiec-Rychter ◽  
Paul Manley ◽  
...  

2013 ◽  
Vol 12 (11) ◽  
pp. 2319-2330 ◽  
Author(s):  
Ningshu Liu ◽  
Bruce R. Rowley ◽  
Cathy O. Bull ◽  
Claudia Schneider ◽  
Andrea Haegebarth ◽  
...  

1983 ◽  
Vol 50 (03) ◽  
pp. 726-730 ◽  
Author(s):  
Hamid Al-Mondhiry ◽  
Virginia McGarvey ◽  
Kim Leitzel

SummaryThis paper reports studies on the interaction between human platelets, the plasma coagulation system, and two human tumor cell lines grown in tissue culture: Melanoma and breast adenocarcinoma. The interaction was monitored through the use of 125I- labelled fibrinogen, which measures both thrombin activity generated by cell-plasma interaction and fibrin/fibrinogen binding to platelets and tumor cells. Each tumor cell line activates both the platelets and the coagulation system simultaneously resulting in the generation of thrombin or thrombin-like activity. The melanoma cells activate the coagulation system through “the extrinsic pathway” with a tissue factor-like effect on factor VII, but the breast tumor seems to activate factor X directly. Both tumor cell lines activate platelets to “make available” a platelet- derived procoagulant material necessary for the conversion of prothrombin to thrombin. The tumor-derived procoagulant activity and the platelet aggregating potential of cells do not seem to be inter-related, and they are not specific to malignant cells.


1989 ◽  
Vol 1 (6) ◽  
pp. 359-365 ◽  
Author(s):  
Richard D. H. Whelan ◽  
Louise K. Hosking ◽  
Alan J. Townsend ◽  
Kenneth H. Cowan ◽  
Bridget T. Hill

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