Article
Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD-transformed hematopoietic cells.
Blood - 15 Mar 2004
Bagrintseva Ksenia, Schwab Ruth, Kohl Tobias M, Schnittger Susanne, Eichenlaub Sabine, Ellwart Joachim W, Hiddemann Wolfgang, Spiekermann Karsten
Abstract excerpt
Activating mutations in the juxtamembrane domain (FLT3-length mutations, FLT3-LM) and in the protein tyrosine kinase domain (TKD) of FLT3 (FLT3-TKD) represent the most frequent genetic alterations in acute myeloid leukemia (AML) and define a molecular target for therapeutic interventions by protein tyrosine kinase (PTK) inhibitors. We could show that distinct activating FLT3-TKD mutations at position D835 mediate...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
