Disabling Abl-perspectives on Abl kinase regulation and cancer therapeutics.
Pharmacologic inhibition of the Bcr-Abl tyrosine kinase in human chronic myeloid leukemia leads to dramatic clinical responses, but relapses occur in advanced stage patients. New findings about Abl kinase domain regulation provide insight into novel strategies for targeted therapy.
Sawyers
Charles L
CL
Department of Medicine, Molecular Biology Institute, UCLA School of Medicine, 90095, USA. csawyers@mednet.ucla.edu
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001549:Benzamides; D001665:Binding Sites; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D016044:Fusion Proteins, bcr-abl; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000201:enzymology; D010879:Piperazines / Q000627:therapeutic use*; D017434:Protein Structure, Tertiary / Q000502:physiology; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors*; D011743:Pyrimidines / Q000627:therapeutic use*
D000970:Antineoplastic Agents; D001549:Benzamides; D004791:Enzyme Inhibitors; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl