[An alternative Abl-kinase inhibitor overcomes imatinib resistance mutations of Bcr-Abl oncogenes].
Von Bubnoff
N
N
III. Medizinische Klinik und Poliklinik, Klinikum rechts der Isar der Technischen Universität München. n.bubnoff@lrz.tum.de
Peschel
C
C
Duyster
J
J
D000818:Animals; D000970:Antineoplastic Agents / Q000737:chemistry / Q000494:pharmacology*; D001549:Benzamides; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D019008:Drug Resistance, Neoplasm / Q000187:drug effects / Q000235:genetics; D004791:Enzyme Inhibitors / Q000737:chemistry / Q000494:pharmacology*; D016313:Genes, abl / Q000187:drug effects*; D006801:Humans; D000068877:Imatinib Mesylate; D051379:Mice; D016297:Mutagenesis, Site-Directed; D010879:Piperazines / Q000737:chemistry / Q000494:pharmacology*; D017354:Point Mutation / Q000187:drug effects; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors*; D011743:Pyrimidines / Q000737:chemistry / Q000494:pharmacology*; D013329:Structure-Activity Relationship
D000970:Antineoplastic Agents; D001549:Benzamides; D004791:Enzyme Inhibitors; C115711:PD 173074; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D011505:Protein-Tyrosine Kinases
Ein alternativer Abl-Kinase-Inhibitor hemmt Imatinib-Resistenzmutationen des Bcr-Abl-Onkogens.