Radiometric assay of cholinesterases in intact tissues in the nanomolar concentration range of acetylcholine

1970 ◽  
Vol 19 (6) ◽  
pp. 2165-2169 ◽  
Author(s):  
S. Ehrenpreis ◽  
T.W. Mittag ◽  
P. Patrick
2013 ◽  
Vol 38 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Yasuhiro Kanbara ◽  
Kazuyoshi Murakane ◽  
Yumiko Nishimura ◽  
Masaya Satoh ◽  
Yasuo Oyama

Blood ◽  
2006 ◽  
Vol 108 (4) ◽  
pp. 1374-1376 ◽  
Author(s):  
Els Lierman ◽  
Cedric Folens ◽  
Elizabeth H. Stover ◽  
Nicole Mentens ◽  
Helen Van Miegroet ◽  
...  

Abstract The FIP1L1-PDGFRA oncogene is a common cause of chronic eosinophilic leukemia (CEL), and encodes an activated tyrosine kinase that is inhibited by imatinib. FIP1L1-PDGFRA–positive patients with CEL respond to low-dose imatinib therapy, but resistance due to acquired T674I mutation has been observed. We report here the identification of sorafenib as a potent inhibitor of the FIP1 like 1–platelet-derived growth factor receptor alpha (FIP1L1-PDGFRα) (T674I) mutant. Sorafenib inhibited the proliferation of FIP1L1-PDGFRα and FIP1L1-PDGFRα(T674I)–transformed Ba/F3 cells and induced apoptosis of the EOL-1 cell line at a low nanomolar concentration. Western blot analysis confirmed that these effects were due to a direct effect on FIP1L1-PDGFRα and FIP1L1-PDGFRα(T674I). Sorafenib was recently approved for the treatment of renal cell carcinoma. Our data suggest that low doses of sorafenib could be efficient for the treatment of FIP1L1-PDGFRA–positive CEL and could be used to overcome resistance to imatinib associated with the T674I mutation.


1975 ◽  
Vol 63 (1) ◽  
pp. 57-61 ◽  
Author(s):  
Bruce E. Haissig ◽  
Arthur L. Schipper

1973 ◽  
Vol 51 (2) ◽  
pp. 618-631 ◽  
Author(s):  
Philip G. Passon ◽  
Jacob D. Peuler

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