title: [Kinase inhibitors against hematological malignancies].
abstract: Dysregulation of protein phosphorylation, especially on tyrosine residues, plays a crucial role in development and progression of hematological malignancies. Since remarkable success in imatinib therapy of CML and Ph+ALL, extensive efforts have made to explore candidate molecular targets and next breakthrough drugs. Now that next generation ABL kinase inhibitors are available for CML, the therapeutic algorithm has been revolutionized. As for AML and lymphoid malignancies, many kinase inhibitors targeting FLT3, BTK and aurora-A are on early and late clinical trials, and a number of promising drugs including ibrutinib are picked up for further evaluation.
authors.forename: Arinobu
authors.initials: A
authors.lastname: Tojo
mesh_terms: D000077329:Agammaglobulinaemia Tyrosine Kinase; D064127:Aurora Kinases / Q000037:antagonists & inhibitors; D019337:Hematologic Neoplasms / Q000188:drug therapy*; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy; D058990:Molecular Targeted Therapy; D010770:Phosphotransferases / Q000037:antagonists & inhibitors*; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D051941:fms-Like Tyrosine Kinase 3 / Q000037:antagonists & inhibitors
chemical_list: D010770:Phosphotransferases; D011505:Protein-Tyrosine Kinases; D051941:fms-Like Tyrosine Kinase 3; D000077329:Agammaglobulinaemia Tyrosine Kinase; C000625949:BTK protein, human; D064127:Aurora Kinases