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Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia

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Konopleva, Marina, Contractor, Rooha, Tsao, Twee, Samudio, Ismael, Ruvolo, Peter P., Kitada, Shinichi, Deng, Xingming, Zhai, Dayong, Shi, Yue-Xi, Sneed, Thomas, Verhaegen, Monique, Soengas, Maria, Ruvolo, Vivian R., McQueen, Teresa, Schober, Wendy D., Watt, Julie C., Jiffar, Tilahun, Ling, Xiaoyang, Marini, Frank C., Harris, David, Dietrich, Martin, Estrov, Zeev, McCubrey, James, May, W. Stratford, Reed, John C., Andreeff, Michael·2006·Cancer Cell
DOI 10.1016/j.ccr.2006.10.006
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Abstract

BCL-2 proteins are critical for cell survival and are overexpressed in many tumors. ABT-737 is a small-molecule BH3 mimetic that exhibits single-agent activity against lymphoma and small-cell lung cancer in preclinical studies. We here report that ABT-737 effectively kills acute myeloid leukemia blast, progenitor, and stem cells without affecting normal hematopoietic cells. ABT-737 induced the disruption of the BCL-2/BAX complex and BAK-dependent but BIM-independent activation of the intrinsic apoptotic pathway. In cells with phosphorylated BCL-2 or increased MCL-1, ABT-737 was inactive. Inhibition of BCL-2 phosphorylation and reduction of MCL-1 expression restored sensitivity to ABT-737. These data suggest that ABT-737 could be a highly effective antileukemia agent when the mechanisms of resistance identified here are considered.

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Cited by

Metadata

Authors
Konopleva, M., Contractor, R., Tsao, T., Samudio, I., Ruvolo, P. P., Kitada, S., Deng, X., Zhai, D., Shi, Y.-X., Sneed, T., Verhaegen, M., Soengas, M., Ruvolo, V. R., McQueen, T., Schober, W. D., Watt, J. C., Jiffar, T., Ling, X., Marini, F. C., Harris, D., Dietrich, M., Estrov, Z., McCubrey, J., May, W. S., Reed, J. C., & Andreeff, M.
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2006-11
Volume
10
Issue
5
Pages
375-388
ISSN
1535-6108 (ISSN-L)
DOI
10.1016/j.ccr.2006.10.006
OpenAlex
W2068962767
Cited by
1,023
References
6
FWCI
20.14
Type
journal article
Language
en
Open access
bronze
Licence

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