Extreme mutational selectivity of axitinib limits its potential use as a targeted therapeutic for BCR-ABL1-positive leukemia

Leukemia. 2016 Jun;30(6):1418-21. doi: 10.1038/leu.2015.318. Epub 2015 Nov 19.

Authors

M S Zabriskie¹, C A Eide^{2

3}, D Yan¹, N A Vellore¹, A D Pomicter¹, S L Savage², B J Druker^{2

3}, M W Deininger^{1

4}, T O'Hare^{1

4}

Affiliations

¹ Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.
² Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
³ Howard Hughes Medical Institute, Portland, OR, USA.
⁴ Division of Hematology and Hematologic Malignancies, University of Utah, Salt Lake City, UT, USA.

No abstract available

Publication types

Letter
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

MeSH terms

Axitinib
Fusion Proteins, bcr-abl / genetics*
Humans
Imidazoles / therapeutic use*
Indazoles / therapeutic use*
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
Mutation / genetics*
Protein Kinase Inhibitors / therapeutic use*

Substances

Imidazoles
Indazoles
Protein Kinase Inhibitors
Axitinib
Fusion Proteins, bcr-abl

Grants and funding