Journal
BLOOD
Volume 118, Issue 8, Pages 2191-2199Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2011-04-351239
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Funding
- American Cancer Society/University of Southern California
- Baxter Foundation
- Concern Foundation
- Nautica Triathlon
- Bogart Foundation
- William Lawrence and Blanche Hughes Foundation
- National Institutes of Health [R01CA137060, R01CA139032, R21CA152497]
- Public Health Service [CA090321]
- University of California-San Francisco Cancer Center
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Relapse of drug-resistant acute lymphoblastic leukemia (ALL) has been associated with increased expression of survivin/BIRC5, an inhibitor of apoptosis protein, suggesting a survival advantage for ALL cells. In the present study, we report that inhibition of survivin in patient-derived ALL can eradicate leukemia. Targeting survivin with shRNA in combination with chemotherapy resulted in no detectable minimal residual disease in a xenograft model of primary ALL. Similarly, pharmacologic knock-down of survivin using EZN-3042, a novel locked nucleic acid antisense oligonucleotide, in combination with chemotherapy eliminated drug-resistant ALL cells. These findings show the importance of survivin expression in drug resistance and demonstrate that survivin inhibition may represent a powerful approach to overcoming drug resistance and preventing relapse in patients with ALL. (Blood. 2011;118(8):2191-2199)
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