Absence of mutations in cereblon (CRBN) and DNA damage-binding protein 1 (DDB1) genes and significance for IMiD therapy

Leukemia. 2014 May;28(5):1129-31. doi: 10.1038/leu.2013.315. Epub 2013 Oct 29.

Authors

A Thakurta¹, A K Gandhi¹, M F Waldman¹, C Bjorklund¹, Y Ning¹, D Mendy¹, P Schafer¹, A Lopez-Girona¹, S Lentzsch², S A Schey³, Y Calle³, R Chelliah³, R Z Orlowski⁴, A Madan⁵, H Avet-Loiseau⁶, R Chopra¹

Affiliations

¹ Translational Development, Celgene Corporation, Summit, NJ, USA.
² Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
³ Department of Haemato-oncology, King's College Hospital and King's College London, London, UK.
⁴ Department of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
⁵ Covance Genomics Laboratory, Seattle, WA, USA.
⁶ Unité de Génomique du Myélome, University Hospital, Toulouse, France.

No abstract available

Publication types

Letter
Research Support, Non-U.S. Gov't

MeSH terms

Adaptor Proteins, Signal Transducing
Adjuvants, Immunologic / therapeutic use*
DNA-Binding Proteins / genetics*
Humans
Lenalidomide
Mutation*
Peptide Hydrolases / genetics*
Thalidomide / analogs & derivatives*
Thalidomide / therapeutic use
Ubiquitin-Protein Ligases

Substances

Adaptor Proteins, Signal Transducing
Adjuvants, Immunologic
CRBN protein, human
DDB1 protein, human
DNA-Binding Proteins
Thalidomide
pomalidomide
Ubiquitin-Protein Ligases
Peptide Hydrolases
Lenalidomide

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