Showing results (31-40 of 163) with videos related to

Sort By:
Pageof 17
Blood|November 14, 1997
The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cellsM W Deininger, J M Goldman, N Lydon, et al.
Nature Reviews. Cancer|July 25, 2012
Pushing the limits of targeted therapy in chronic myeloid leukaemiaThomas O'Hare, Matthew S Zabriskie, Anna M Eiring, et al.
Experimental Hematology|March 18, 2006
Establishment of a murine model of aggressive systemic mastocytosis/mast cell leukemiaShadmehr Demehri, Amie Corbin, Marc Loriaux, et al.
British Journal of Haematology|December 19, 1998
The susceptibility of Philadelphia chromosome positive cells to FAS-mediated apoptosis is not linked to the tyrosine kinase activity of BCR-ABLJ Gora-Tybor, M W Deininger, J M Goldman, et al.
Experimental Hematology|October 31, 2003
Comparative gene expression profile of chronic myeloid leukemia cells innately resistant to imatinib mesylateAlex J Tipping, Michael W Deininger, John M Goldman, et al.
Leukemia|June 13, 2008
Bruton's tyrosine kinase is not essential for Bcr-Abl-mediated transformation of lymphoid or myeloid cellsM MacPartlin, A M Smith, B J Druker, et al.
Experimental Hematology|May 17, 2000
The tyrosine kinase inhibitor STI571, like interferon-alpha, preferentially reduces the capacity for amplification of granulocyte-macrophage progenitors from patients with chronic myeloid leukemiaS B Marley, M W Deininger, R J Davidson, et al.
Blood|December 9, 2004
RNAi-induced down-regulation of FLT3 expression in AML cell lines increases sensitivity to MLN518Denise K Walters, Eric P Stoffregen, Michael C Heinrich, et al.
The Journal of Clinical Investigation|December 16, 2010
Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activityAmie S Corbin, Anupriya Agarwal, Marc Loriaux, et al.
Cancer Research|April 15, 2000
BCR-ABL tyrosine kinase activity regulates the expression of multiple genes implicated in the pathogenesis of chronic myeloid leukemiaM W Deininger, S Vieira, R Mendiola, et al.
Pageof 17