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Cancer Cell. 2016 Apr 11;29(4):423-425. doi: 10.1016/j.ccell.2016.03.017.

Deletion Mutations Keep Kinase Inhibitors in the Loop.

Author information

1
Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA; Cancer Biology Institute, Yale University, West Haven, CT 06516, USA.
2
Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA.
3
Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA; Cancer Biology Institute, Yale University, West Haven, CT 06516, USA. Electronic address: mark.lemmon@yale.edu.

Abstract

Effective clinical application of conformationally selective kinase inhibitors requires tailoring drug choice to the tumor's activating mutation(s). In this issue of Cancer Cell, Foster et al. (2016) describe how activating deletions in BRAF, EGFR, and HER2 cause primary resistance to common inhibitors, suggesting strategies for improved inhibitor selection.

PMID:
27070691
PMCID:
PMC5028821
DOI:
10.1016/j.ccell.2016.03.017
[Indexed for MEDLINE]
Free PMC Article

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