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

摘要: Numerous studies have revealed that the BCR-ABL oncoprotein abnormally engages a multitude of signaling pathways, some which may be important for its leukemogenic properties. Central to this has been determination tyrosine kinase function is mainly responsible transforming potential, and can targeted with small molecule inhibitors, such as imatinib mesylate (Gleevec, STI-571). Despite apparent success, development clinical resistance therapy, inability eradicate BCR-ABL-positive malignant hematopoietic progenitors demand detailed investigations additional effector pathways CML treatment. The promotion cellular survival via suppression apoptotic fundamental characteristic tumor cells enables anti-cancer therapies. As substrates kinases Akt, FoxO family transcription factors, particularly FoxO3a, emerged playing an role in cell cycle arrest apoptosis cells. This review will discuss our current understanding focus on suppressive mechanisms alternative approaches well potential factors novel therapeutic targets.