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BCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability

Oncogene volume 21, pages 8591–8604 (2002)Cite this article

Abstract

BCR/ABL regulates cell proliferation, apoptosis, differentiation and adhesion. In addition, BCR/ABL can induce resistance to cytostatic drugs and irradiation by modulation of DNA repair mechanisms, cell cycle checkpoints and Bcl-2 protein family members. Upon DNA damage BCR/ABL not only enhances reparation of DNA lesions (e.g. homologous recombination repair), but also prolongs activation of cell cycle checkpoints (e.g. G2/M) providing more time for repair of otherwise lethal lesions. Moreover, by modification of anti-apoptotic members of the Bcl-2 family (e.g. upregulation of Bcl-xL) BCR/ABL provides a cytoplasmic ‘umbrella’ protecting mitochondria from the ‘rain’ of apoptotic signals coming from the damaged DNA in the nucleus, thus preventing release of cytochrome c and activation of caspases. The unrepaired and/or aberrantly repaired (but not lethal) DNA lesions resulting from spontaneous and/or drug-induced damage can accumulate in BCR/ABL-transformed cells leading to genomic instability and malignant progression of the disease. Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and, in combination with standard chemotherapeutics can exert strong anti-leukemia effect.

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Acknowledgements

This work was supported by grants from NIH/NCI and American Cancer Society. T Skorski is a Scholar of the Leukemia and Lymphoma Society. Special thanks for Michal O Nowicki, whose computer skills were helpful during preparations of the figures.

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    Tomasz Skorski

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Skorski, T. BCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability. Oncogene 21, 8591–8604 (2002). https://doi.org/10.1038/sj.onc.1206087

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