Journal
CANCER CONTROL
Volume 16, Issue 2, Pages 100-107Publisher
H LEE MOFFITT CANCER CENTER & RESEARCH INST
DOI: 10.1177/107327480901600202
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Background: The fusion protein BCR-ABL results in constitutive tyrosine kinase activity. It also affects downstream targets as well as the subcellular location of the normally tightly regulated Abl tyrosine kinase. Methods: The authors review the current knowledge concerning the signaling networks associated with BCR-ABL-dependent transformation. Results: Although BCR-ABL is considered a single genetic change, the dysregulated tyrosine kinase activates a network of signals that contributes to cytokine-independent growth, resistance to apoptosis, and genetic instability. Conclusions: The effectiveness of BCR-ABL-dependent transformation of hematopoietic stem cells is due not to a single pathway but rather to the culmination of a network of signaling pathways.
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