NDLI: BCL-2 dependence and ABT-737 sensitivity in acute lymphoblastic leukemia

Content Provider	PubMed Central
Author	Moore, Victoria Del Gaizo Schlis, Krysta D. Sallan, Stephen E. Armstrong, Scott A. Anthony, Letai
Copyright Year	2008
Abstract	Cancer cells acquire disruptions in normal signal transduction pathways and homeostatic mechanisms that would trigger apoptosis in normal cells. These abnormalities include genomic instability, oncogene activation, and growth factor independent proliferation. Therefore, cancer cells likely require a block in apoptosis in order to survive. Overexpression of the antiapoptotic protein BCL-2 provides a block in apoptosis that is frequently observed in cancer cells. We have developed methods for the detection and analysis of BCL-2 dependence and here apply them to acute lymphoblastic leukemia (ALL). BH3 profiling, a mitochondrial assay that classifies blocks in the intrinsic apoptotic pathway, indicated a dependence on BCL-2 of both ALL cell lines and primary samples. This dependence predicted that BCL-2 would be complexed with select pro-death BH3 family proteins, a prediction confirmed by the isolation of BCL-2 complexes with BIM. Furthermore, the BH3 profiling and protein analysis predicted that ALL cell lines and primary cells would be sensitive to ABT-737 as a single agent. Finally, BH3 profiling and protein studies accurately predicted a relative degree of sensitivity to BCL-2 antagonism in cell lines. The ALL cells studied exhibit BCL-2 dependence, supporting clinical trials of BCL-2 antagonists in ALL as single agents or combination therapies.
Related Links	http://dx.doi.org/10.1182/blood-2007-06-098012
Ending Page	2309
Page Count	10
Starting Page	2300
File Format	PDF
ISSN	00064971
e-ISSN	15280020
Journal	Blood
Issue Number	4
Volume Number	111
Language	English
Publisher	American Society of Hematology
Publisher Date	2008-02-15
Access Restriction	Open
Rights Holder	American Society of Hematology
Subject Keyword	Immunology Cell Biology Biochemistry Hematology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Hematology Biochemistry Immunology

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