Abstract
The Leukaemias are a group of cancers affecting the white blood cell system. Chronic myeloid leukaemia (CML) is characterised by a reciprocal translocation between chromosomes 9 and 22 resulting in the production of the BCR-ABL protein tyrosine kinase. Expression of BCR-ABL in stem cells of the myeloid blood cell population has been shown to be directly responsible for malignant transformation. We identified down-regulation of the negative growth regulator, CCN3, as a consequence of BCR-ABL expression. Investigations have shown CCN3 functions to inhibit cell growth and survival whilst promoting apoptosis; our findings suggest that BCR-ABL utilises CCN3 down-regulation to escape growth control. Further understanding of CCN3 mechanisms are required to develop new therapeutic strategies targeting this pathway.
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Acknowledgements
The authors wish to acknowledge financial support from the following: Leukaemia Research Fund (UK), Northern Ireland Leukaemia Research Fund and the Elimination of Leukaemia Fund.
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McCallum, L., Irvine, A.E. (2010). CCN3: A NOVel Growth Factor in Leukaemia. In: Perbal, A., Takigawa, M., Perbal, B. (eds) CCN Proteins in Health and Disease. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-3779-4_16
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DOI: https://doi.org/10.1007/978-90-481-3779-4_16
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