期刊
BLOOD
卷 126, 期 21, 页码 2366-2369出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2015-07-567958
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资金
- National Institutes of Health, National Heart, Lung, and Blood Institute [R01HL082945]
- National Cancer Institute [P01CA108631, F30CA199988-01]
- Edward P. Evans Foundation
- Gabrielle's Angel Foundation
- Leukemia and Lymphoma Society Scholar Award
- National Institute of General Medical Sciences [T32GM007753, T32GM722639]
Lenalidomide acts by a novel drug mechanism-modulation of the substrate specificity of the CRL4(CRBN) E3 ubiquitin ligase. In multiple myeloma, lenalidomide induces the ubiquitination of IKZF1 and IKZF3 by CRL4 CRBN. Subsequent proteasomal degradation of these transcription factors kills multiple myeloma cells. In del(5q) myelodysplastic syndrome, lenalidomide induces the degradation of CK1a, which preferentially affects del(5q) cells because they express this gene at haploinsufficient levels. In the future, modulation of ubiquitin ligase function may enable us to target previously undruggable proteins.
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