Targeting FLT3 kinase in acute myelogenous leukemia: progress, perils, and prospects.
Activating mutations of the FLT3 receptor tyrosine kinase are the most common recurring genetic abnormality in acute myelogenous leukemia (AM). Inhibition of FLT3 kinase activity by small molecule inhibitors has been proposed as a novel therapeutic approach AML. The pre-clinical and clinical development of candidate FLT3 inhibitors will be reviewed.
Heinrich
Michael C
MC
Division of Hematology and Medical Oncology, Oregon Health & Science University Cancer Institute; and Portland VA Medical Center, Portland, OR 97201, USA. heinrich@ohsu.edu
D000818:Animals; D002986:Clinical Trials as Topic; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics; D009154:Mutation; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors*; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors* / Q000235:genetics; D016896:Treatment Outcome; D051941:fms-Like Tyrosine Kinase 3
D004791:Enzyme Inhibitors; D011518:Proto-Oncogene Proteins; C497970:FLT3 protein, human; D020794:Receptor Protein-Tyrosine Kinases; D051941:fms-Like Tyrosine Kinase 3