scholarly journals Reduced Folate Carrier Gene Silencing in Multiple Antifolate-resistant Tumor Cell Lines Is Due to a Simultaneous Loss of Function of Multiple Transcription Factors but Not Promoter Methylation

2003 ◽  
Vol 279 (1) ◽  
pp. 374-384 ◽  
Author(s):  
Lilah Rothem ◽  
Michal Stark ◽  
Yotam Kaufman ◽  
Lior Mayo ◽  
Yehuda G. Assaraf
2006 ◽  
Vol 97 (3) ◽  
pp. 530-543 ◽  
Author(s):  
Kouji Katabami ◽  
Takumi Kato ◽  
Rikio Sano ◽  
Masaharu Ogura ◽  
Hiromi Mizuno ◽  
...  

2011 ◽  
Vol 44 (13) ◽  
pp. S205
Author(s):  
Hosseini Ahmad ◽  
Rahnama Susan ◽  
Jaberipour Mansooreh ◽  
Habib-Agahi Mojtaba

2016 ◽  
Author(s):  
Stephen Bridgett ◽  
James Campbell ◽  
Christopher J. Lord ◽  
Colm J. Ryan

AbstractGenes whose function is selectively essential in the presence of cancer associated genetic aberrations represent promising targets for the development of precision therapeutics. Here we present CancerGD (www.cancergd.org), a resource that integrates genotypic profiling with large-scale loss-of-function genetic screens in tumor cell lines to identify such genetic dependencies. CancerGD provides tools for searching, visualizing, and interpreting these genetic dependencies through the integration of functional interaction networks.


Life Sciences ◽  
2003 ◽  
Vol 73 (15) ◽  
pp. 1963-1972 ◽  
Author(s):  
Ze-Jun Liu ◽  
Masato Maekawa ◽  
Toshinobu Horii ◽  
Motoki Morita

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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