Mechanisms of Transformation by the BCR/ABL Oncogene
Copyright policy )Mechanisms of Transformation by the BCR/ABL Oncogene
The Philadelphia chromosome generates a chimeric oncogene in which the BCR and c-ABL genes are fused. The product of this oncogene, BCR/ABL, has elevated ABL tyrosine kinase activity, relocates to the cytoskeleton, and phosphorylates multiple cellular substrates. BCR/ABL transforms hematopoietic cells and exerts a wide variety of biological effects, including reduction in growth factor dependence, enhanced viability, and altered adhesion of chronic myelocytic leukemia (CML) cells. Elevated tyrosine kinase activity of BCR/ABL is critical for activating downstream signal transduction and for all aspects of transformation. This review will describe mechanisms of transformation by the BCR/ABL oncogene and opportunities for clinical intervention with specific signal transduction inhibitors such as STI-571 in CML.
- Brigham and Women's Faulkner Hospital United States
- Dana-Farber Cancer Institute United States
- Harvard University United States
Oncogene Proteins, Fusion, Fusion Proteins, bcr-abl, Models, Biological, Piperazines, Protein Structure, Tertiary, Enzyme Activation, Protein Transport, Cell Transformation, Neoplastic, Pyrimidines, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Benzamides, Imatinib Mesylate, Humans, Philadelphia Chromosome, Enzyme Inhibitors, Phosphorylation, Reactive Oxygen Species, Protein Processing, Post-Translational, Cytoskeleton, Signal Transduction
Oncogene Proteins, Fusion, Fusion Proteins, bcr-abl, Models, Biological, Piperazines, Protein Structure, Tertiary, Enzyme Activation, Protein Transport, Cell Transformation, Neoplastic, Pyrimidines, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Benzamides, Imatinib Mesylate, Humans, Philadelphia Chromosome, Enzyme Inhibitors, Phosphorylation, Reactive Oxygen Species, Protein Processing, Post-Translational, Cytoskeleton, Signal Transduction
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