title: Structure, function, and resistance in chronic myeloid leukemia.
abstract: Chronic myeloid leukemia (CML) is effectively treated by tyrosine kinase inhibitors (TKIs). Rarely, CML cases develop TKI resistance through acquisition of compound mutations. In this issue of Cancer Cell, Zabriskie and colleagues study how structural changes caused by compound mutations cause clinically relevant changes in TKI sensitivity.
authors.affiliation: Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA. Electronic address: jradich@fhcrc.org.
authors.forename: Jerald
authors.initials: J
authors.lastname: Radich
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics*; D011724:Pyridazines / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; D007093:Imidazoles; D011724:Pyridazines; C545373:ponatinib; D016044:Fusion Proteins, bcr-abl