FoxO tumor suppressors and BCR-ABL-induced leukemia: a matter of evasion of apoptosis.

ABSTRACT: Numerous studies have revealed that the BCR-ABL oncoprotein abnormally engages a multitude of signaling pathways, some of which may be important for its leukemogenic properties. Central to this has been the determination that the tyrosine kinase function of BCR-ABL is mainly responsible for its transforming potential, and can be targeted with small molecule inhibitors, such as imatinib mesylate (Gleevec, STI-571). Despite this apparent success, the development of clinical resistance to imatinib therapy, and the inability of imatinib to eradicate BCR-ABL-positive malignant hematopoietic progenitors demand detailed investigations of additional effector pathways that can be targeted for CML treatment. The promotion of cellular survival via the suppression of apoptotic pathways is a fundamenta

SUBMITTER: Jagani Z 

PROVIDER: S-EPMC2180393 | biostudies-literature | 2008 Jan

REPOSITORIES: biostudies-literature