Deletion Mutations Keep Kinase Inhibitors in the Loop

Daniel M Freed; Jin H Park; Ravi Radhakrishnan; Mark A Lemmon

doi:10.1016/j.ccell.2016.03.017

Deletion Mutations Keep Kinase Inhibitors in the Loop

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

Authors

Daniel M Freed¹, Jin H Park¹, Ravi Radhakrishnan², Mark A Lemmon³

Affiliations

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: [email protected].

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.

Publication types

Comment

MeSH terms

Carcinoma, Non-Small-Cell Lung / drug therapy
Drug Resistance, Neoplasm / genetics
ErbB Receptors / genetics
Humans
Lung Neoplasms / genetics
Mutation*
Neoplasms / genetics*
Protein Kinase Inhibitors / pharmacology
Sequence Deletion

Substances

Protein Kinase Inhibitors
ErbB Receptors

Grants and funding

U54 CA193417/CA/NCI NIH HHS/United States